OL3-Buffers.docx - CHEM 163 General Chemistry III Bellevue ...
Conjugate Definition in Chemistry - ThoughtCo
conjugate solution meaning in chemistry
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Comprehensive DD on $CTYX: The OTC Biotech Stock of the Decade That Is Being Slept On
[Connectyx (OTC-PINK: CTYX). Will change to Curative Biotechnology with ticker $CURB in Q1 2021.] I posted this on pennystocks yesterday. Full Disclosure: I have a $6k initial position in this stock at a cost average of $.06. The stock is now at $0.155 (as of 2/6/21) with my position at $15.5k and movement is just starting. I am not a financial advisor. I am simply a broke graduate student interested in investing and fucking retiring early. This post represents my personal views and should not be taken as financial advice. Do your own damn research and stop pumping your hard-earned cash into trending stocks on Reddit posts that are nothing but hype, rocket emojis, and a mob chat jerking each other off. Also, not a doctor! The medical content below should never be a substitute for professional medical advice. With that said, $CTYX is going to fucking Pluto 🚀🚀🚀🚀🚀🚀 🌑 Price Target: $0.5 by May 1, 2021; $1.25 - $3.00 (~10x) within 2 years with credible potential to be listed on NASDAQ. This company is absolutely solid on all sides: healthy financials, an experienced & reliable management team, favorable market conditions with a reasonable business model, a solid lineup of products in its pipeline, and many large announcements anticipated within the next 3 months. Simply put, there is extreme asymmetric upside. $CTYX or Connectyx was taken over by its current team led by CEO Paul Michaels around Feb 2020. Within a year, this CEO has kept every promise he's made and established the infrastructure for growth. The company specializes in bringing orphan drugs (more on this below) through clinical trials and then to market. Paul and his team have decades of experience in big pharma, biotech research, finance, and drug licensing/development (in-depth description in the Management Team section below). They've vetted 3 promising drug candidates in under a year and promised to start clinical trials by mid-2022. If any one of these pass phase 1/2 trials, the market cap grows by hundreds of millions. They also have a reasonable chance to obtain a Priority Review Voucher (PRV) from the FDA that is worth $100-$300M from their strategic picks. They have a clean balance sheet, acquired non-dilute bridge financing while putting these drugs through trials, and have plans of additional deals in the near future. Why orphan drugs? Orphan drugs are therapeutics that treat rare diseases (defined as illnesses affecting less than 200k Americans per year). From the Orphan Drug Act, there are multiple incentives given by the government to develop orphan drugs: (1) significant tax credits (2) longer market exclusivity after approval (3) waiver of certain FDA fees (4) easier & faster approval process. In 2019, the global orphan drug market is estimated to be valued at $151B. By 2027, this is projected to reach $340.84B (10% compounded annual growth). This the cornerstone of their business model. By gathering a group of experts, they can cheaply vet high potential candidates to add to their development pipeline and then commercialize them from reduced fees as well as fast-track benefits from the FDA. So why the hell is it call Connectyx? It is just the old name of a software services company which the team acquired. The company has filed for a name change that will be granted within the next 2 weeks to Curative Biotechnology Inc. with a new ticker $CURB. In addition, the CEO himself has hinted at an uplisting to $OTCQB (a certification upgrade from current pink sheet status), mergeacquisition announcements, and $100M in non-dilutive funding. The official FINRA announcement of the name change will be the catalyst for the additional news. Some quick notes about the charts. The 15x jump in the past couple of months is only the beginning. There is a clear trend of resistance breakthroughs and medium-term consolidation after each announcement. Volatility is low, the number of outstanding shares is small, and there is limited dilutive potential for an OTC. Let's dive deeper into this hidden gem. All-Star Management Team CEO Paul Michaels Curative BioTech lucked out with a CEO with 25 years of experience in investment banking with a focus on life sciences. Paul has an impressive record, starting as the Executive Vice President and board member of Global Capital Group (a Wall Street wealth management firm). He also got extensive experience in big Pharma through Inabata & Co. Ltd, a subsidiary of a large Japanese drug company, Sumitomo Chemical Group, which totaled $21.8B in revenue in 2013 and employs over 30k people. While serving as Inabata's CFO, Paul licensed American drugs (some from Gilead) for the Asian market. After, the guy helped create Nobelpharma, an orphan drug company, which licenses drugs for rare diseases and got over $35M in initial capital. In February 2020, Paul took over Connectyx (a software services company at the time) and made it an orphan drug company. It is extremely rare for pink-sheet companies to have such high-caliber, established talent as a leader: decades of experience with finance and leadership positions in multi-billion dollar pharmaceutical companies. He helped build up Inabata and Nobelpharam (both thriving today), and I am confident in his ability to do it again with Connectyx. VP Communications Pam Bisikirski Recently, Curative announced Pam as the new Vice President of Communications. She previously served as the director of marketing of National Vision for 21 years. National Vision ($EYE) is a huge optical retail, eye care, and eye-ware company that is trading near a $4B market cap on NASDAQ. Scientific Advisory Board Dr. Michael Grace [news] - Ph.D. in Biochemistry and BS in Chemistry from the University of Nebraska. 30 years of experience in BioPharma with top roles in names like Procter & Gamble, Schering-Plough, Bristol-Myers Squibb, NPS Pharma, and Advaxis Immunotherapies. Lead 6 products to registration and commercialization. Dr. Ronald Bordens [news] - Ph.D. in Biotechnology with over 26 publications and over 2000 citations. 40 years in biotech and big pharma in research & development. Had a fruitful 26-year career at Schering-Plough Research. Richard Garr [news] - Serves as Director and CEO as well as President of Neuralstem Inc. (now Seneca Biopharma, Inc. which is listed on NASDAQ as $SNCA) for 20 years. Advocate for right to try treatments in the US and Europe. Founded Access Hope CRO (contract research organization) which dedicates itself to this cause. Was founder and current Board Member of the First Star Foundation Mid-Atlantic chapter which focuses on ill children (including pediatric brain cancer). Robust Drug Pipeline Keep in mind this company became a biotech firm in Feb 2020 and they already have 3 drugs in the pipeline along with exclusive rights licenses. Insane. 1) IMT504 immune therapy to treat late-stage rabies. (11/23/2020 Announcement implies IMT504 rabies license deal is complete) Strategic relationship with Mid-Atlantic BioTherapeutics, Inc. announced on 8/27/2020. Acquired all rights for development of this patented immunotherapy to treat late-stage rabies (a disease with 100% fatality rate after the treatable period, [kills 59k](https://www.ncbi.nlm.nih.gov/pmc/articles/PMC6613553/#:~:text=about this topic%3F-,Each year%2C rabies causes approximately 59%2C000 deaths worldwide%2C including approximately,of postexposure prophylaxis (PEP).).)) globally per year). Now, the value of this may not be in the drug approval itself (although passing trials would be a huge asset of course). The value is the potential in CTYX obtaining a Priority Review Voucher (PRV). These coupons are handed out by the FDA each year to incentivize research into rare diseases. Exercising the coupon means diminishing the approval process from 10 months to 6 after trials. Further, you can freely sell these on a secondary market to other companies! Historically, these have been sold between $100M to $300M each. If obtained, this is an instant 2x-6x increase to its current $50M market cap. There's more.. notice that the FDA has added Rabies to its PRV-eligible tropical diseases list. Currently, there is only a handful of rabies therapies being researched. This means there's actually a good chance of CYTX getting rewarded a voucher, despite the relatively low count of vouchers distributed annually. PRVs are also possible for all other drugs in the pipeline. 2) CURB906 monoclonal antibody cytotoxic conjugate for the treatment of Glioblastoma. (10/16/2020 NIH gives a grant of license for worldwide rights) The second license was filed near July 2020 for a novel monoclonal antibody conjugate to treat brain cancer. Glioblastomas are aggressive brain tumors with poor survival rates in children. Recent studies (e.g. s1, s2) have shown different combinations of chemo-therapy and antibody-drug conjugate (ADCs) therapeutics were effective in both mice and human models. ADCs are innovative methods that attach a cytotoxic compound (one meant to kill cancer cells) to an antibody that specifically attaches to certain cancer cell receptors, thus delivering therapies to their targets. There is great promise and lots of potential in these therapeutics. Exclusive Evaluation and Commercialization Option License Agreement with the National Cancer Institute (NCI) has been granted. 3) Metformin repurposed to treat retinal degeneration. (2/4/2021 NIH gives a grant of license for worldwide rights) This is probably the ace in the hole and the largest reason behind the recent stock surge. On 2/4/2021, CTYX announced they received an NIH grant for exclusive worldwide rights to adapt a diabetes drug, Metformin, to treat retinal degeneration. Not only is Metformin proven safe (it is a widely used drug to treat Type1 Diabetes since 1995), there are many studies (e.g. s1, s2, s3) that hint at its effectiveness for retinal diseases. The recently granted license not only covers pediatric retinal generation (in the form of Stargardt Disease), it covers treatment in adults as well and includes macular degeneration. This promising treatment potentially covers 2/3 of the US population (2/3 of Americans are pre-diabetic, 1/10 are diabetic, and 11 million have some form of macular degeneration; why care about diabetes? diabetes causes retinopathy). Huge Upcoming Announcements The announced name change is the opening of the flood gates for all upcoming news. Additional licenses, uplistings, and deals with be done under the new company name. Expect many of these announcements following FINRA approval. These are some forward-looking implications:
(Within 2 weeks) FINRA approval of name change to Curative Biotechnology Inc. and ticker $CURB.
(Within weeks of name change) Following the name change, there will be an uplisting to OTCQB. OTCQB is a tier up from Pink Sheets and must adhere to stricter management certifications, undergo annual audits, and are more stringent in their financial reporting. Connectyx is currently working to become fully reporting OTCQB; to that end, the Company appointed Jonathan D. Leinwand, PA as Legal Counsel.
(Within weeks of name change) Talk of multiple upcoming drugs (if the Metformin announcement was one of them, we should see at least one more).
(Within weeks of name change) Hints at $100M of non-dilutive funding for clinical trials.
(Within months of name change) Mergers, acquisitions, and partnerships with other firms for licensing and commercialization.
Downsides Before we get ahead of ourselves and dream about retiring in 3 months while riding this into space, we gotta ground ourselves and discuss the downsides. Remember: in life, there are no solutions, only tradeoffs. There are always downsides and risks. Risk 1) This is currently a pink sheet. That itself should make you more cautious because there is reduced regulation, more "flexible" rules, and less scrutiny/transparency. Risk 2) High risk, high reward. If all 3 drugs flop (assuming no additional therapeutics are added) and they don't get a PRV (priority review voucher), then this company is worthless. Granted, the chances are low, but still a possibility to consider. Risk 3) Share dilution and raising capital. Because clinical trials often require obscene amounts of capital (~$400M investment for normal drugs), there is a risk that managers might dilute the stock in order to raise money or to take profits in general. There are currently 322M outstanding shares with 1.1B authorized shares. Read the share disclosures, do the math, gauge the risks. Note that orphan drug trials are a lot less costly as well. Risks and unknowns are certainly there. However, the upside potential is too big to ignore. Buy at pennies, sell for dollars. Do the research and take advantage of any dips that might come on Monday from 2 days of green explosions. ------------------------------------------------------------ TL;DR.
You should fucking read it, because this Phoenix has a high probability of rising from ashes to become the OTC stock of the yeadecade with effortless 10x upside in the short-term.
$CTYX will change to $CURB (Curative BioTech) soon. Business strategy: (1) bring together financial experts, veterans in big pharma, accomplished biotech researchers, and world-class grant writers to vet orphan drugs (2) make deals and obtain licenses for these drugs to help get them through clinical trials (3) take advantage of special FDA benefits for orphan drug approval (faster approval process, fee waivers, etc) and commercialize them after with longer exclusive rights.
Finance: company has no problematic debt, clean sheets, non-dilutive funding, and a small number of outstanding shares for an OTC (322M).
Products: 3 promising drug candidates in the pipeline within a year. Multiple exclusive license grants approved by the NIH.
Upcoming Announcements: (1) name change (2) uplisting to $OTCQB from pink sheets (3) more non-dilutive funding (4) additional drug(s) in pipeline (5) mergers, acquisitions, and deals with other pharma companies.
Current market cap: $50M. Upside: (1) +$100M - $300M if awarded a priority review voucher (PRV) (2) +hundreds of millions in market cap if any of the 3 promising drugs goes past phase 2 ~end of 2022 (3) +millions in speculative capital if new drugs are announced in pipeline (4) potential future merger with large pharma or uplisting to NASDAQ (other biotech companies are listed with half the number of products).
Comprehensive DD on $CTYX: The OTC Biotech Stock of the Decade That Is Being Slept On
[Connectyx (OTC-PINK: CTYX). Will change to Curative Biotechnology with ticker $CURB in Q1 2021.] Full Disclosure: I have a $6k initial position in this stock at a cost average of $.06. The stock is now at $0.155 (as of 2/6/21) with my position at $15.5k and movement is just starting. I am not a financial advisor. I am simply a broke graduate student interested in investing and fucking retiring early. This post represents my personal views and should not be taken as financial advice. Do your own damn research and stop pumping your hard-earned cash into trending stocks on Reddit posts that are nothing but hype, rocket emojis, and a mob chat jerking each other off. Also, not a doctor! The medical content below should never be a substitute for professional medical advice. With that said, $CTYX is going to fucking Pluto 🚀🚀🚀🚀🚀🚀 🌑 Price Target: $0.5 by May 1, 2021; $1.25 - $3.00 (~10x) within 2 years with credible potential to be listed on NASDAQ. This company is absolutely solid on all sides: healthy financials, an experienced & reliable management team, favorable market conditions with a reasonable business model, a solid lineup of products in its pipeline, and many large announcements anticipated within the next 3 months. Simply put, there is extreme asymmetric upside. $CTYX or Connectyx was taken over by its current team led by CEO Paul Michaels around Feb 2020. Within a year, this CEO has kept every promise he's made and established the infrastructure for growth. The company specializes in bringing orphan drugs (more on this below) through clinical trials and then to market. Paul and his team have decades of experience in big pharma, biotech research, finance, and drug licensing/development (in-depth description in the Management Team section below). They've vetted 3 promising drug candidates in under a year and promised to start clinical trials by mid-2022. If any one of these pass phase 1/2 trials, the market cap grows by hundreds of millions. They also have a reasonable chance to obtain a Priority Review Voucher (PRV) from the FDA that is worth $100-$300M from their strategic picks. They have a clean balance sheet, acquired non-dilute bridge financing while putting these drugs through trials, and have plans of additional deals in the near future. Why orphan drugs? Orphan drugs are therapeutics that treat rare diseases (defined as illnesses affecting less than 200k Americans per year). From the [Orphan Drug Act](https://www.wikiwand.com/en/Orphan_Drug_Act_of_1983#:~:text=The Orphan Drug Act of,residing in the United States.)), there are multiple incentives given by the government to develop orphan drugs: (1) significant tax credits (2) longer market exclusivity after approval (3) waiver of certain FDA fees (4) easier & faster approval process. In 2019, the global orphan drug market is estimated to be valued at $151B. By 2027, this is projected to reach $340.84B (10% compounded annual growth). This the cornerstone of their business model. By gathering a group of experts, they can cheaply vet high potential candidates to add to their development pipeline and then commercialize them from reduced fees as well as fast-track benefits from the FDA. So why the hell is it call Connectyx? It is just the old name of a software services company which the team acquired. The company has filed for a name change that will be granted within the next 2 weeks to Curative Biotechnology Inc. with a new ticker $CURB. In addition, the CEO himself has hinted at an uplisting to $OTCQB (a certification upgrade from current pink sheet status), mergeacquisition announcements, and $100M in non-dilutive funding. The official FINRA announcement of the name change will be the catalyst for the additional news. Some quick notes about the charts. The 15x jump in the past couple of months is only the beginning. There is a clear trend of resistance breakthroughs and medium-term consolidation after each announcement. Volatility is low, the number of outstanding shares is small, and there is limited dilutive potential for an OTC. Let's dive deeper into this hidden gem.
All-Star Management Team
CEO Paul Michaels Curative BioTech lucked out with a CEO with 25 years of experience in investment banking with a focus on life sciences. Paul has an impressive record, starting as the Executive Vice President and board member of Global Capital Group (a Wall Street wealth management firm). He also got extensive experience in big Pharma through [Inabata & Co. Ltd's](https://www.wikiwand.com/en/Inabata_%26_Co.,_Ltd.)), a subsidiary of a large Japanese drug company, Sumitomo Chemical Group, which totaled $21.8B in revenue in 2013 and employs over 30k people. While serving as Inabata's CFO, Paul licensed American drugs (some from Gilead) for the Asian market. After, the guy helped create Nobelpharma, an orphan drug company, which licenses drugs for rare diseases and got over $35M in initial capital. In February 2020, Paul took over Connectyx (a software services company at the time) and made it an orphan drug company. It is extremely rare for pink-sheet companies to have such high-caliber, established talent as a leader: decades of experience with finance and leadership positions in multi-billion dollar pharmaceutical companies. He helped build up Inabata and Nobelpharam (both thriving today), and I am confident in his ability to do it again with Connectyx. VP Communications Pam Bisikirski Recently, Curative announced Pam as the new Vice President of Communications. She previously served as the director of marketing of National Vision for 21 years. National Vision ($EYE) is a huge optical retail, eye care, and eye-ware company that is trading near a $4B market cap on NASDAQ. Scientific Advisory Board Dr. Michael Grace [news] - Ph.D. in Biochemistry and BS in Chemistry from the University of Nebraska. 30 years of experience in BioPharma with top roles in names like Procter & Gamble, Schering-Plough, Bristol-Myers Squibb, NPS Pharma, and Advaxis Immunotherapies. Lead 6 products to registration and commercialization. Dr. Ronald Bordens [news] - Ph.D. in Biotechnology with over 26 publications and over 2000 citations. 40 years in biotech and big pharma in research & development. Had a fruitful 26-year career at Schering-Plough Research. Richard Garr [news] - Serves as Director and CEO as well as President of Neuralstem Inc. (now Seneca Biopharma, Inc. which is listed on NASDAQ as $SNCA) for 20 years. Advocate for right to try treatments in the US and Europe. Founded Access Hope CRO (contract research organization) which dedicates itself to this cause. Was founder and current Board Member of the First Star Foundation Mid-Atlantic chapter which focuses on ill children (including pediatric brain cancer).
Robust Drug Pipeline
Keep in mind this company became a biotech firm in Feb 2020 and they already have 3 drugs in the pipeline along with exclusive rights licenses. Insane. 1) IMT504 immune therapy to treat late-stage rabies. (11/23/2020 Announcement implies IMT504 rabies license deal is complete) Strategic relationship with Mid-Atlantic BioTherapeutics, Inc. announced on 8/27/2020. Acquired all rights for development of this patented immunotherapy to treat late-stage rabies (a disease with 100% fatality rate after the treatable period, [kills 59k](https://www.ncbi.nlm.nih.gov/pmc/articles/PMC6613553/#:~:text=about this topic%3F-,Each year%2C rabies causes approximately 59%2C000 deaths worldwide%2C including approximately,of postexposure prophylaxis (PEP).).)) globally per year). Now, the value of this may not be in the drug approval itself (although passing trials would be a huge asset of course). The value is the potential in CTYX obtaining a Priority Review Voucher (PRV). These coupons are handed out by the FDA each year to incentivize research into rare diseases. Exercising the coupon means diminishing the approval process from 10 months to 6 after trials. Further, you can freely sell these on a secondary market to other companies! Historically, these have been sold between $100M to $300M each. If obtained, this is an instant 2x-6x increase to its current $50M market cap. There's more.. notice that the FDA has added Rabies to its PRV-eligible tropical diseases list. Currently, there is only a handful of rabies therapies being researched. This means there's actually a good chance of CYTX getting rewarded a voucher, despite the relatively low count of vouchers distributed annually. PRVs are also possible for all other drugs in the pipeline. 2) CURB906 monoclonal antibody cytotoxic conjugate for the treatment of Glioblastoma. (10/16/2020 NIH gives a grant of license for worldwide rights) The second license was filed near July 2020 for a novel monoclonal antibody conjugate to treat brain cancer. Glioblastomas are aggressive brain tumors with poor survival rates in children. Recent studies (e.g. s1, s2) have shown different combinations of chemo-therapy and antibody-drug conjugate (ADCs) therapeutics were effective in both mice and human models. ADCs are innovative methods that attach a cytotoxic compound (one meant to kill cancer cells) to an antibody that specifically attaches to certain cancer cell receptors, thus delivering therapies to their targets. There is great promise and lots of potential in these therapeutics. Exclusive Evaluation and Commercialization Option License Agreement with the National Cancer Institute (NCI) has been granted. 3) Metformin repurposed to treat retinal degeneration. (2/4/2021 NIH gives a grant of license for worldwide rights) This is probably the ace in the hole and the largest reason behind the recent stock surge. On 2/4/2021, CTYX announced they received an NIH grant for exclusive worldwide rights to adapt a diabetes drug, Metformin, to treat retinal degeneration. Not only is Metformin proven safe (it is a widely used drug to treat Type1 Diabetes since 1995), there are many studies (e.g. s1, s2, s3) that hint at its effectiveness for retinal diseases. The recently granted license not only covers pediatric retinal generation (in the form of Stargardt Disease), it covers treatment in adults as well and includes macular degeneration. This promising treatment potentially covers 2/3 of the US population (2/3 of Americans are pre-diabetic, 1/10 are diabetic, and 11 million have some form of macular degeneration; why care about diabetes? diabetes causes retinopathy).
Huge Upcoming Announcements
The announced name change is the opening of the flood gates for all upcoming news. Additional licenses, uplistings, and deals with be done under the new company name. Expect many of these announcements following FINRA approval. These are some forward-looking implications:
(Within 2 weeks) FINRA approval of name change to Curative Biotechnology Inc. and ticker $CURB.
(Within weeks of name change) Following the name change, there will be an uplisting to OTCQB. OTCQB is a tier up from Pink Sheets and must adhere to stricter management certifications, undergo annual audits, and are more stringent in their financial reporting. Connectyx is currently working to become fully reporting OTCQB; to that end, the Company appointed Jonathan D. Leinwand, PA as Legal Counsel.
(Within weeks of name change) Talk of multiple upcoming drugs (if the Metformin announcement was one of them, we should see at least one more).
(Within weeks of name change) Hints at $100M of non-dilutive funding for clinical trials.
(Within months of name change) Mergers, acquisitions, and partnerships with other firms for licensing and commercialization.
Downsides
Before we get ahead of ourselves and dream about retiring in 3 months while riding this into space, we gotta ground ourselves and discuss the downsides. Remember: in life, there are no solutions, only tradeoffs. There are always downsides and risks. Risk 1) This is currently a pink sheet. That itself should make you more cautious because there is reduced regulation, more "flexible" rules, and less scrutiny/transparency. Risk 2) High risk, high reward. If all 3 drugs flop (assuming no additional therapeutics are added) and they don't get a PRV (priority review voucher), then this company is worthless. Granted, the chances are low, but still a possibility to consider. Risk 3) Share dilution and raising capital. Because clinical trials often require obscene amounts of capital (~$400M investment for normal drugs), there is a risk that managers might dilute the stock in order to raise money or to take profits in general. There are currently 322M outstanding shares with 1.1B authorized shares. Read the share disclosures, do the math, gauge the risks. Note that orphan drug trials are a lot less costly as well. Risks and unknowns are certainly there. However, the upside potential is too big to ignore. Buy at pennies, sell for dollars. Do the research and take advantage of any dips that might come on Monday from 2 days of green explosions. ------------------------------------------------------------ TL;DR.
You should fucking read it, because this Phoenix has a high probability of rising from ashes to become the OTC stock of the yeadecade with effortless 10x upside in the short-term.
$CTYX will change to $CURB (Curative BioTech) soon. Business strategy: (1) bring together financial experts, veterans in big pharma, accomplished biotech researchers, and world-class grant writers to vet orphan drugs (2) make deals and obtain licenses for these drugs to help get them through clinical trials (3) take advantage of special FDA benefits for orphan drug approval (faster approval process, fee waivers, etc) and commercialize them after with longer exclusive rights.
Finance: company has no problematic debt, clean sheets, non-dilutive funding, and a small number of outstanding shares for an OTC (322M).
Products: 3 promising drug candidates in the pipeline within a year. Multiple exclusive license grants approved by the NIH.
Upcoming Announcements: (1) name change (2) uplisting to $OTCQB from pink sheets (3) more non-dilutive funding (4) additional drug(s) in pipeline (5) mergers, acquisitions, and deals with other pharma companies.
Current market cap: $50M. Upside: (1) +$100M - $300M if awarded a priority review voucher (PRV) (2) +hundreds of millions in market cap if any of the 3 promising drugs goes past phase 2 ~end of 2022 (3) +millions in speculative capital if new drugs are announced in pipeline (4) potential future merger with large pharma or uplisting to NASDAQ (other biotech companies are listed with half the number of products).
Comprehensive DD on $CTYX: The OTC Biotech Stock of the Decade That Is Being Slept On
[Connectyx (OTC-PINK: CTYX). Will change to Curative Biotechnology with ticker $CURB in Q1 2021.] Full Disclosure: I have a $6k initial position in this stock at a cost average of $.06. The stock is now at $0.155 (as of 2/6/21) with my position at $15.5k and movement is just starting. I am not a financial advisor. I am simply a broke graduate student interested in investing and fucking retiring early. This post represents my personal views and should not be taken as financial advice. Do your own damn research and stop pumping your hard-earned cash into trending stocks on Reddit posts that are nothing but hype, rocket emojis, and a mob chat jerking each other off. Also, not a doctor! The medical content below should never be a substitute for professional medical advice. With that said, $CTYX is going to fucking Pluto 🚀🚀🚀🚀🚀🚀 🌑 Price Target: $0.5 by May 1, 2021; $1.25 - $3.00 (~10x) within 2 years with credible potential to be listed on NASDAQ. This company is absolutely solid on all sides: healthy financials, an experienced & reliable management team, favorable market conditions with a reasonable business model, a solid lineup of products in its pipeline, and many large announcements anticipated within the next 3 months. Simply put, there is extreme asymmetric upside. $CTYX or Connectyx was taken over by its current team led by CEO Paul Michaels around Feb 2020. Within a year, this CEO has kept every promise he's made and established the infrastructure for growth. The company specializes in bringing orphan drugs (more on this below) through clinical trials and then to market. Paul and his team have decades of experience in big pharma, biotech research, finance, and drug licensing/development (in-depth description in the Management Team section below). They've vetted 3 promising drug candidates in under a year and promised to start clinical trials by mid-2022. If any one of these pass phase 1/2 trials, the market cap grows by hundreds of millions. They also have a reasonable chance to obtain a Priority Review Voucher (PRV) from the FDA that is worth $100-$300M from their strategic picks. They have a clean balance sheet, acquired non-dilute bridge financing while putting these drugs through trials, and have plans of additional deals in the near future. Why orphan drugs? Orphan drugs are therapeutics that treat rare diseases (defined as illnesses affecting less than 200k Americans per year). From the [Orphan Drug Act](https://www.wikiwand.com/en/Orphan_Drug_Act_of_1983#:~:text=The Orphan Drug Act of,residing in the United States.)), there are multiple incentives given by the government to develop orphan drugs: (1) significant tax credits (2) longer market exclusivity after approval (3) waiver of certain FDA fees (4) easier & faster approval process. In 2019, the global orphan drug market is estimated to be valued at $151B. By 2027, this is projected to reach $340.84B (10% compounded annual growth). This the cornerstone of their business model. By gathering a group of experts, they can cheaply vet high potential candidates to add to their development pipeline and then commercialize them from reduced fees as well as fast-track benefits from the FDA. So why the hell is it call Connectyx? It is just the old name of a software services company which the team acquired. The company has filed for a name change that will be granted within the next 2 weeks to Curative Biotechnology Inc. with a new ticker $CURB. In addition, the CEO himself has hinted at an uplisting to $OTCQB (a certification upgrade from current pink sheet status), mergeacquisition announcements, and $100M in non-dilutive funding. The official FINRA announcement of the name change will be the catalyst for the additional news. Some quick notes about the charts. The 15x jump in the past couple of months is only the beginning. There is a clear trend of resistance breakthroughs and medium-term consolidation after each announcement. Volatility is low, the number of outstanding shares is small, and there is limited dilutive potential for an OTC. Let's dive deeper into this hidden gem. All-Star Management Team CEO Paul Michaels Curative BioTech lucked out with a CEO with 25 years of experience in investment banking with a focus on life sciences. Paul has an impressive record, starting as the Executive Vice President and board member of Global Capital Group (a Wall Street wealth management firm). He also got extensive experience in big Pharma through [Inabata & Co. Ltd's](https://www.wikiwand.com/en/Inabata_%26_Co.,_Ltd.)), a subsidiary of a large Japanese drug company, Sumitomo Chemical Group, which totaled $21.8B in revenue in 2013 and employs over 30k people. While serving as Inabata's CFO, Paul licensed American drugs (some from Gilead) for the Asian market. After, the guy helped create Nobelpharma, an orphan drug company, which licenses drugs for rare diseases and got over $35M in initial capital. In February 2020, Paul took over Connectyx (a software services company at the time) and made it an orphan drug company. It is extremely rare for pink-sheet companies to have such high-caliber, established talent as a leader: decades of experience with finance and leadership positions in multi-billion dollar pharmaceutical companies. He helped build up Inabata and Nobelpharam (both thriving today), and I am confident in his ability to do it again with Connectyx. VP Communications Pam Bisikirski Recently, Curative announced Pam as the new Vice President of Communications. She previously served as the director of marketing of National Vision for 21 years. National Vision ($EYE) is a huge optical retail, eye care, and eye-ware company that is trading near a $4B market cap on NASDAQ. Scientific Advisory Board Dr. Michael Grace [news] - Ph.D. in Biochemistry and BS in Chemistry from the University of Nebraska. 30 years of experience in BioPharma with top roles in names like Procter & Gamble, Schering-Plough, Bristol-Myers Squibb, NPS Pharma, and Advaxis Immunotherapies. Lead 6 products to registration and commercialization. Dr. Ronald Bordens [news] - Ph.D. in Biotechnology with over 26 publications and over 2000 citations. 40 years in biotech and big pharma in research & development. Had a fruitful 26-year career at Schering-Plough Research. Richard Garr [news] - Serves as Director and CEO as well as President of Neuralstem Inc. (now Seneca Biopharma, Inc. which is listed on NASDAQ as $SNCA) for 20 years. Advocate for right to try treatments in the US and Europe. Founded Access Hope CRO (contract research organization) which dedicates itself to this cause. Was founder and current Board Member of the First Star Foundation Mid-Atlantic chapter which focuses on ill children (including pediatric brain cancer). Robust Drug Pipeline Keep in mind this company became a biotech firm in Feb 2020 and they already have 3 drugs in the pipeline along with exclusive rights licenses. Insane. 1) IMT504 immune therapy to treat late-stage rabies. (11/23/2020 Announcement implies IMT504 rabies license deal is complete) Strategic relationship with Mid-Atlantic BioTherapeutics, Inc. announced on 8/27/2020. Acquired all rights for development of this patented immunotherapy to treat late-stage rabies (a disease with 100% fatality rate after the treatable period, [kills 59k](https://www.ncbi.nlm.nih.gov/pmc/articles/PMC6613553/#:~:text=about this topic%3F-,Each year%2C rabies causes approximately 59%2C000 deaths worldwide%2C including approximately,of postexposure prophylaxis (PEP).).)) globally per year). Now, the value of this may not be in the drug approval itself (although passing trials would be a huge asset of course). The value is the potential in CTYX obtaining a Priority Review Voucher (PRV). These coupons are handed out by the FDA each year to incentivize research into rare diseases. Exercising the coupon means diminishing the approval process from 10 months to 6 after trials. Further, you can freely sell these on a secondary market to other companies! Historically, these have been sold between $100M to $300M each. If obtained, this is an instant 2x-6x increase to its current $50M market cap. There's more.. notice that the FDA has added Rabies to its PRV-eligible tropical diseases list. Currently, there is only a handful of rabies therapies being researched. This means there's actually a good chance of CYTX getting rewarded a voucher, despite the relatively low count of vouchers distributed annually. PRVs are also possible for all other drugs in the pipeline. 2) CURB906 monoclonal antibody cytotoxic conjugate for the treatment of Glioblastoma. (10/16/2020 NIH gives a grant of license for worldwide rights) The second license was filed near July 2020 for a novel monoclonal antibody conjugate to treat brain cancer. Glioblastomas are aggressive brain tumors with poor survival rates in children. Recent studies (e.g. s1, s2) have shown different combinations of chemo-therapy and antibody-drug conjugate (ADCs) therapeutics were effective in both mice and human models. ADCs are innovative methods that attach a cytotoxic compound (one meant to kill cancer cells) to an antibody that specifically attaches to certain cancer cell receptors, thus delivering therapies to their targets. There is great promise and lots of potential in these therapeutics. Exclusive Evaluation and Commercialization Option License Agreement with the National Cancer Institute (NCI) has been granted. 3) Metformin repurposed to treat retinal degeneration. (2/4/2021 NIH gives a grant of license for worldwide rights) This is probably the ace in the hole and the largest reason behind the recent stock surge. On 2/4/2021, CTYX announced they received an NIH grant for exclusive worldwide rights to adapt a diabetes drug, Metformin, to treat retinal degeneration. Not only is Metformin proven safe (it is a widely used drug to treat Type1 Diabetes since 1995), there are many studies (e.g. s1, s2, s3) that hint at its effectiveness for retinal diseases. The recently granted license not only covers pediatric retinal generation (in the form of Stargardt Disease), it covers treatment in adults as well and includes macular degeneration. This promising treatment potentially covers 2/3 of the US population (2/3 of Americans are pre-diabetic, 1/10 are diabetic, and 11 million have some form of macular degeneration; why care about diabetes? diabetes causes retinopathy). Huge Upcoming Announcements The announced name change is the opening of the flood gates for all upcoming news. Additional licenses, uplistings, and deals with be done under the new company name. Expect many of these announcements following FINRA approval. These are some forward-looking implications:
(Within 2 weeks) FINRA approval of name change to Curative Biotechnology Inc. and ticker $CURB.
(Within weeks of name change) Following the name change, there will be an uplisting to OTCQB. OTCQB is a tier up from Pink Sheets and must adhere to stricter management certifications, undergo annual audits, and are more stringent in their financial reporting. Connectyx is currently working to become fully reporting OTCQB; to that end, the Company appointed Jonathan D. Leinwand, PA as Legal Counsel.
(Within weeks of name change) Talk of multiple upcoming drugs (if the Metformin announcement was one of them, we should see at least one more).
(Within weeks of name change) Hints at $100M of non-dilutive funding for clinical trials.
(Within months of name change) Mergers, acquisitions, and partnerships with other firms for licensing and commercialization.
Downsides Before we get ahead of ourselves and dream about retiring in 3 months while riding this into space, we gotta ground ourselves and discuss the downsides. Remember: in life, there are no solutions, only tradeoffs. There are always downsides and risks. Risk 1) This is currently a pink sheet. That itself should make you more cautious because there is reduced regulation, more "flexible" rules, and less scrutiny/transparency. Risk 2) High risk, high reward. If all 3 drugs flop (assuming no additional therapeutics are added) and they don't get a PRV (priority review voucher), then this company is worthless. Granted, the chances are low, but still a possibility to consider. Risk 3) Share dilution and raising capital. Because clinical trials often require obscene amounts of capital (~$400M investment for normal drugs), there is a risk that managers might dilute the stock in order to raise money or to take profits in general. There are currently 322M outstanding shares with 1.1B authorized shares. Read the share disclosures, do the math, gauge the risks. Note that orphan drug trials are a lot less costly as well. Risks and unknowns are certainly there. However, the upside potential is too big to ignore. Buy at pennies, sell for dollars. Do the research and take advantage of any dips that might come on Monday from 2 days of green explosions. ------------------------------------------------------------ TL;DR.
You should fucking read it, because this Phoenix has a high probability of rising from ashes to become the OTC stock of the yeadecade with effortless 10x upside in the short-term.
$CTYX will change to $CURB (Curative BioTech) soon. Business strategy: (1) bring together financial experts, veterans in big pharma, accomplished biotech researchers, and world-class grant writers to vet orphan drugs (2) make deals and obtain licenses for these drugs to help get them through clinical trials (3) take advantage of special FDA benefits for orphan drug approval (faster approval process, fee waivers, etc) and commercialize them after with longer exclusive rights.
Finance: company has no problematic debt, clean sheets, non-dilutive funding, and a small number of outstanding shares for an OTC (322M).
Products: 3 promising drug candidates in the pipeline within a year. Multiple exclusive license grants approved by the NIH.
Upcoming Announcements: (1) name change (2) uplisting to $OTCQB from pink sheets (3) more non-dilutive funding (4) additional drug(s) in pipeline (5) mergers, acquisitions, and deals with other pharma companies.
Current market cap: $50M. Upside: (1) +$100M - $300M if awarded a priority review voucher (PRV) (2) +hundreds of millions in market cap if any of the 3 promising drugs goes past phase 2 ~end of 2022 (3) +millions in speculative capital if new drugs are announced in pipeline (4) potential future merger with large pharma or uplisting to NASDAQ (other biotech companies are listed with half the number of products).
[https://pubchem.ncbi.nlm.nih.gov/periodic-table/png/Periodic_Table_of_Elements_w_Chemical_Group_Block_PubChem.png ] or [https://ptable.com/#Properties ] If we are going off the Lewis definition of acids as electron pair acceptors and bases as electron pair donors, the problems of ion solubility (mostly H+ and OH- ions) can be appropriately distanced from the actual behavior of hydronium (H3O+) or hydroxide (OH-) complexes in water. In other words, we first ask what species exist in what concentrations in the solution of interest, then what will happen between the different species. However, we cannot completely separate the Brønsted-Lowry and Lewis definitions due to Le Chatelier’s principle, which would state that the presence of the products of dissociation tend to prevent additional dissociation events. However, if product ions start being consumed in other reactions, the effective result is to shift the equilibrium back towards the starting materials, and additional dissociation events will then become energetically favorable. The result of this is that the behavior of chemical reactions is best contemplated holistically and with a full set of executive functionality instead of being taught as a series of disconnected fragments that imply the existence of a much higher level of precision than is actually ever possible and must be stitched together by students working without the benefit of fully developed brains. As I go through the process of writing out this series of posts, I am getting the definite impression that the progress that has been made in our understanding of atoms and orbitals has mostly obsoleted the way that general chemistry is currently taught, and that the current state of teaching is centered around exams to the detriment of the students. My general chemistry education also had far too much emphasis on the Brønsted-Lowry definition of acids and bases instead of treating these as equilibrium problems. So and before we go any farther, let’s get pH out of the way. A lowercase “p” denotes the mathematical operation of taking the negative log of a quantity for some reason, so pH is actually the negative (base 10) log of H where H is the ionic activity of “H+” in the solution of interest. As it turns out, this is actually the activity of hydronium complexes instead of lone protons, but unless you are trying to visualize what is actually happening in the solution the two can be treated as equivalent. Of course, if you’ve gotten so obsessed with applying equations to chemical processes that you are willing to ignore the three-dimensional picture, you’re probably also not doing anything of value, but anyway. In most cases, pH can be calculated with the concentration of hydronium in moles per liter instead of a more rigorous activity measurement, so in other words pH is mostly equal to -log([H3O+]). [I should also note that the difference between the concentration of hydronium and the concentration of protons is not particularly significant in acid-base problems because the protons in water will either react with other species or form hydronium. If you are calculating the concentration of protons in water at any given time, you are also calculating the concentration of hydronium.] If you’re willing to get pedantic there is a nearly infinite amount of additional complexity that can be brought in here, but I’m not emotionally invested in this and see no reason to care. Proceeding with pH=-([H3O+]), you may notice that we are only calculating the acidity of our solution and not the basicity. However, due to the spontaneous dissociation/autoionization of water, acidity and basicity are closely related to each other. In a volume of water, the multiplication product of the concentrations in moles per liter of hydronium/H3O+ and hydroxide/OH- is a constant. At 25 degrees Celsius, this constant (Kw) is equal to 1.0x10^-14, and Kw=[H3O+]*[OH-]. In this notation scheme, the square brackets denote concentration in moles per liter, and square brackets are usually but not always moles per liter. In any case, the reason to care is that the assumptions here mostly hold true once we start adding additional chemical species to the volume of water we started with. As the number of ions in solution increase, other issues start to arise, but mostly what you need to remember is that this is a simplified model and not an absolute definition of what is happening on the molecular level. Where this model is valuable is in relating the concentration of hydronium to the concentration of hydroxide (both in moles per liter) in a mostly reliable manner, which means that if we know a value for one at a given time we can calculate the value of the other one. So, if you have a concentration of hydroxide and you want to know the pH, you can use Kw to calculate the concentration of hydronium, then take the negative base 10 log of the result to get to pH. The addition of the logarithm allows the comparison of numbers with vastly different orders of magnitude but also brings quite a bit of confusion. In any case, using these assumptions we can define interrelated pH and pOH scales to measure acidity and basicity as the density of hydronium and hydroxide in solution. You may notice that this aligns well with the Lewis definitions, although we are not considering any other possible Lewis acids or bases. Once you get into organic chemistry and start trying to do reactions, having a trace amount of ions in your reaction mixture doesn’t get you anywhere, and all of the assumptions as previously defined get thrown out of the window. At high concentrations of ions/high ionic activities (which are mostly equivalent concepts), we get back to the idiosyncratic and non-intuitive behavior that we expect to see in chemistry. These conditions also favor the Lewis definitions, and if it seems like I am being a bit heavy-handed in mentioning the advantages of teaching the Lewis definitions to students as early as possible you would be quite correct. Fully embracing the Lewis definitions will require the more neurotic or tradition-bound individuals among the chemical community to let go of literally centuries of work that turns out not to be valid, but as before I have no particular emotional investment in Brønsted-Lowry and would much prefer to be taught the concepts in a way that actually makes sense. In my list of topics I am supposed to cover acid-base equilibrium, which in the context of water (aqueous solutions) is how hydronium and hydroxide move into and out of solution. First looking at “HA” or a proton donor, we can either have the acidic proton attached to the conjugate base or not. The Lewis basic strength of “A-” determines how tightly the H+ is bonded and therefore how accessible it is to the surrounding water molecules. If the H+ is bonded too tightly, there is no chance of a water molecule ever removing it, and the compound is probably not going to be participating in any aqueous acid-base reactions. At this point I am really wanting to bring in some more organic chemistry concepts and talk about an example like ethanol (CH3CH2OH) as a compound with three distinct types of protons in three different chemical environments, with the hydrogen on the oxygen end (Eth-OH) as well as the two lone pairs on the oxygen being the most interesting electron pair acceptors and donors, but the current general chemistry syllabus as defined by the American Chemical Society (ACS) prevents this. Moving on to “BOH” in water, the strength of the bond between “B+” and hydroxide is also going to be important. As an example, the hydroxl group on ethanol has essentially no chance of being removed in an aqueous solution unless something quite energetic/violent happens, but the hydroxl proton can be stripped off or another proton can bond to one of the lone pairs on oxygen depending on the reaction conditions. In the context of this post, I am basically trying to get into a decent position to talk about buffers. These are modeled by the Henderson Hasselbalch equation and are usually a combination of a weakly proton-donating “HA” with the “A-” part of that molecule paired with a positively charged counterion (counter-cation possibly). As an example cation, let’s choose sodium (Na+), which is a terrible electron pair acceptor because it is already in a noble gas valence electron configuration and adding electrons will be destabilizing. So, we can basically ignore the sodium ions unless we are interested in the total ionic activity for some reason, and at the same time the charges all balance out. If we select the correct “A-” and adjust the relative amounts of “HA” and “NaA”, we end up with a mixture that starts out at a pH that can be predicted via calculation. This is normal when adding proton or hydroxide donors to water, but where buffers are different is the ability to absorb proton or hydroxide inputs without the pH changing much. This is because of the presence of both protonated “HA” and deprotonated “A-” and is useful in situations were the molecules under study cannot tolerate large pH swings, which usually means proteins and other biological molecules. Selecting a buffer requires the concept of the constant of acidic dissociation (Ka) and the negative log of the same (pKa), but between this and Henderson Hasselbalch equation you should have plenty of keywords to play with. I am also supposed to be covering titrations here, but since these are as obsolete as Brønsted-Lowry and really shitty to have to carry out in the lab I’m not going to bother.
i.e. 20 glucose molecules linked together would have 19 bonds
Molecular formula
# of molecules * molecular formula - number of bonds * H20 (from hydrolysis)
i.e. when you bond 5 glucose molecules together you have to subtract 4H2O
pH/pOH
-log[H+] = pH
-log[OH-] = pOH
pH + pOH = 14
Leaf surface area
i.e. using graph paper to find surface area
Transpiration rate
Amount of water used / surface area / time
Labs
Transpiration Lab
Basically you take this potometer which measures the amount of water that gets sucked up by a plant that you have and you expose the plant to different environmental conditions (light, humidity, temperature) and see how fast the water gets transpired
Random stuff to know:
It’s hard to get it to work properly
A tight seal of vaseline keeps everything tidy and prevents water from evaporating straight from the tube, also allows for plant to suck properly
Water travels from high water potential to low water potential
2) Cell Structure & Function
Content
Cellular Components
Many membrane-bound organelles evolved from once free prokaryotes via endosymbiosis, such as mitochondria (individual DNA)
Compartmentalization allows for better SA:V ratio and helps regulate cellular processes
Cytoplasm: thick solution in each cell containing water, salts, proteins, etc; everything - nucleus
Cytoplasmic streaming: moving all the organelles around to give them nutrients, speeds up reactions
Cytosol: liquid of the cytoplasm (mostly water)
Plasma Membrane: separates inside of cell from extracellular space, controls what passes through amphipathic area (selectively permeable)
Aquaporin: hole in membrane that allows water through
Cell Wall: rigid polysaccharide layer outside of plasma membrane in plants/fungi/bacteria
Bacteria have peptidoglycan, fungi have chitin, and plants have cellulose and lignin
Turgor pressure pushes the membrane against the wall
Nucleus: contains genetic information
Has a double membrane called the nuclear envelope with pores
Nucleolus: in nucleus, produces ribosomes
Chromosomes: contain DNA
Centrioles: tubulin thing that makes up centrosome in the middle of a chromosome
Smooth Endoplasmic Reticulum: storage of proteins and lipids
Rough Endoplasmic Reticulum: synthesizes and packages proteins
Chloroplasts: photosynthetic, sunlight transferred into chemical energy and sugars
More on this in photosynthesis
Vacuoles: storage, waste breakdown, hydrolysis of macromolecules, plant growth
Plasmodesmata: channels through cell walls that connect adjacent cells
Golgi Apparatus: extracellular transport
Lysosome: degradation and waste management
Mutations in the lysosome cause the cell to swell with unwanted molecules and the cell will slow down or kill itself
Mitochondria: powerhouse of the cell
Mutations in the mitochondria cause a lack of deficiency of energy in the cell leading to an inhibition of cell growth
Vesicles: transport of intracellular materials
Microtubules: tubulin, stiff, mitosis, cell transport, motor proteins
Microfilaments: actin, flexible, cell movement
Flagella: one big swim time
Cilia: many small swim time
Peroxisomes: bunch of enzymes in a package that degrade H202 with catalase
Ribosomes: protein synthesis
Microvilli: projections that increase cell surface area like tiny feetsies
In the intestine, for example, microvilli allow more SA to absorb nutrients
Cytoskeleton: hold cell shape
Cellular Transport
Passive transport: diffusion
Cell membranes selectively permeable (large and charged repelled)
Tonicity: osmotic (water) pressure gradient
Cells are small to optimize surface area to volume ratio, improving diffusion
Primary active transport: ATP directly utilized to transport
Secondary active transport: something is transported using energy captured from movement of other substance flowing down the concentration gradient
Endocytosis: large particles enter a cell by membrane engulfment
Phagocytosis: “cell eating”, uses pseudopodia around solids and packages it within a membrane
Pinocytosis: “cell drinking”, consumes droplets of extracellular fluid
Receptor-mediated endocytosis: type of pinocytosis for bulk quantities of specific substances
Exocytosis: internal vesicles fuse with the plasma membrane and secrete large molecules out of the cell
Ion channels and the sodium potassium pump
Ion channel: facilitated diffusion channel that allows specific molecules through
Sodium potassium pump: uses charged ions (sodium and potassium)
Membrane potential: voltage across a membrane
Electrogenic pump: transport protein that generates voltage across a membrane
Proton pump: transports protons out of the cell (plants/fungi/bacteria)
Cotransport: single ATP-powered pump transports a specific solute that can drive the active transport of several other solutes
Bulk flow: one-way movement of fluids brought about by pressure
Dialysis: diffusion of solutes across a selective membrane
Cellular Components Expanded: The Endomembrane System
Nucleus + Rough ER + Golgi Bodies
Membrane and secretory proteins are synthesized in the rough endoplasmic reticulum, vesicles with the integral protein fuse with the cis face of the Golgi apparatus, modified in Golgi, exits as an integral membrane protein of the vesicles that bud from the Golgi’s trans face, protein becomes an integral portion of that cell membrane
Calculations
Surface area to volume ratio of a shape (usually a cube)
U-Shaped Tube (where is the water traveling)
Solution in u-shaped tube separated by semi-permeable membrane
find average of solute (that is able to move across semi permeable membrane)
add up total molar concentration on both sides
water travels where concentration is higher
Water Potential = Pressure Potential + Solute Potential
Solute Potential = -iCRT
i = # of particles the molecule will make in water
C = molar concentration
R = pressure constant (0.0831)
T = temperature in kelvin
Labs
Diffusion and Osmosis
Testing the concentration of a solution with known solutions
Dialysis bag
Semipermeable bag that allows the water to pass through but not the solute
Potato core
Has a bunch of solutes inside
Relevant Experiments
Lynne Margolis: endosymbiotic theory (mitochondria lady)
Chargaff: measured A/G/T/C in everything (used UV chromatography)
Franklin + Watson and Crick: discovered structure of DNA; Franklin helped with x ray chromatography
3) Cellular Energetics
Content
Reactions and Thermodynamics
Baseline: used to establish standard for chemical reaction
Catalyst: speeds up a reaction (enzymes are biological catalysts)
Exergonic: energy is released
Endergonic: energy is consumed
Coupled reactions: energy lost/released from exergonic reaction is used in endergonic one
Laws of Thermodynamics:
First Law: energy cannot be created nor destroyed, and the sum of energy in the universe is constant
Second Law: energy transfer leads to less organization (greater entropy)
Third Law: the disorder (entropy) approaches a constant value as the temperature approaches 0
Cellular processes that release energy may be coupled with other cellular processes
Loss of energy flow means death
Energy related pathways in biological systems are sequential to allow for a more controlled/efficient transfer of energy (product of one metabolic pathway is reactant for another)
Bioenergetics: study of how energy is transferred between living things
Fuel + 02 = CO2 + H20
Combustion, Photosynthesis, Cellular Respiration (with slight differences in energy)
Enzymes
Speed up chemical processes by lowering activation energy
Structure determines function
Active sites are selective
Enzymes are typically tertiary- or quaternary-level proteins
Catabolic: break down / proteases and are exergonic
Anabolic: build up and are endergonic
Enzymes do not change energy levels
Substrate: targeted molecules in enzymatic
Many enzymes named by ending substrate in “-ase”
Enzymes form temporary substrate-enzyme complexes
Enzymes remain unaffected by the reaction they catalyze
Enzymes can’t change a reaction or make other reactions occur
Induced fit: enzyme has to change its shape slightly to accommodate the substrate
Cofactor: factor that help enzymes catalyze reactions (org or inorg)
Examples: temp, pH, relative ratio of enzyme and substrate
Organic cofactors are called coenzymes
Denaturation: enzymes damaged by heat or pH
Regulation: protein’s function at one site is affected by the binding of regulatory molecule to a separate site
Enzymes enable cells to achieve dynamic metabolism - undergo multiple metabolic processes at once
Cannot make an endergonic reaction exergonic
Steps to substrates becoming products
Substrates enters active site, enzyme changes shape
Substrates held in active site by weak interactions (i.e. hydrogen bonds)
Substrates converted to product
Product released
Active site available for more substrate
Rate of enzymatic reaction increases with temperature but too hot means denaturation
Inhibitors fill the active site of enzymes
Some are permanent, some are temporary
Competitive: block substrates from their active sites
Non competitive (allosteric): bind to different part of enzyme, changing the shape of the active site
Allosteric regulation: regulatory molecules interact with enzymes to stimulate or inhibit activity
Enzyme denaturation can be reversible
Cellular Respiration
Steps
Glycolysis
Acetyl co-A reactions
Krebs / citric acid cycle
Oxidative phosphorylation
Brown fat: cells use less efficient energy production method to make heat
Absorption vs action spectrum (broader, cumulative, overall rate of photosynthesis)
Components
Chloroplast
Mesophyll: interior leaf tissue that contains chloroplasts
Pigment: substance that absorbs light
Steps
Light-Dependent Reaction
Light-Independent (Dark) Reaction (Calvin Cycle)
Anaerobic Respiration (Fermentation)
Glycolysis yields 2ATP + 2NADH + 2 Pyruvate
2NADH + 2 Pyruvate yields ethanol and lactate
Regenerates NAD+
Calculations
Calculate products of photosynthesis & cellular respiration
Labs
Enzyme Lab
Peroxidase breaks down peroxides which yields oxygen gas, quantity measured with a dye
Changing variables (i.e. temperature) yields different amounts of oxygen
Photosynthesis Lab
Vacuum in a syringe pulls the oxygen out of leaf disks, no oxygen causes them to sink in bicarbonate solution, bicarbonate is added to give the disks a carbon source for photosynthesis which occurs at different rates under different conditions, making the disks buoyant
Cellular Respiration Lab
Use a respirometer to measure the consumption of oxygen (submerge it in water)
You put cricket/animal in the box that will perform cellular respiration
You put KOH in the box with cricket to absorb the carbon dioxide (product of cellular respiration)-- it will form a solid and not impact your results
Relevant Experiments
Engelmann
Absorption spectra dude with aerobic bacteria
4) Cell Communication & Cell Cycle
Content
Cell Signalling
Quorum sensing: chemical signaling between bacteria
See Bonnie Bassler video
Taxis/Kinesis: movement of an organism in response to a stimulus (chemotaxis is response to chemical)
Ligand: signalling molecule
Receptor: ligands bind to elicit a response
Hydrophobic: cholesterol and other such molecules can diffuse across the plasma membrane
Hydrophilic: ligand-gated ion channels, catalytic receptors, G-protein receptor
Signal Transduction
Process by which an extracellular signal is transmitted to inside of cell
Pathway components
Signal/Ligand
Receptor protein
Relay molecules: second messengers and the phosphorylation cascade
DNA response
Proteins in signal transduction can cause cancer if activated too much (tumor)
RAS: second messenger for growth factor-- suppressed by p53 gene (p53 is protein made by gene) if it gets too much
Response types
Gene expression changes
Cell function
Alter phenotype
Apoptosis- programmed cell death
Cell growth
Secretion of various molecules
Mutations in proteins can cause effects downstream
Pathways are similar and many bacteria emit the same chemical within pathways, evolution!
Feedback
Positive feedback amplifies responses
Onset of childbirth, lactation, fruit ripening
Negative feedback regulates response
Blood sugar (insulin goes down when glucagon goes up), body temperature
Cell cycle
Caused by reproduction, growth, and tissue renewal
Checkpoint: control point that triggers/coordinates events in cell cycle
Mitotic spindle: microtubules and associated proteins
Cytoskeleton partially disassembles to provide the material to make the spindle
Elongates with tubulin
Shortens by dropping subunits
Aster: radial array of short microtubules
Kinetochores on centrosome help microtubules to attach to chromosomes
Broke apart liver cells and realized the significance of the signal transduction pathway, as the membrane and the cytoplasm can’t activate glycogen phosphorylase by themselves
5) Heredity
Content
Types of reproduction
Sexual: two parents, mitosis/meiosis, genetic variation/diversity (and thus higher likelihood of survival in a changing environment)
Asexual: doesn’t require mate, rapid, almost genetically identitical (mutations)
Binary fission (bacteria)
Budding (yeast cells)
Fragmentation (plants and sponges)
Regeneration (starfish, newts, etc.)
Meiosis
One diploid parent cell undergoes two rounds of cell division to produce up to four haploid genetically varied cells
n = 23 in humans, where n is the number of unique chromosomes
Meiosis I
Prophase: synapsis (two chromosome sets come together to form tetrad), chromosomes line up with homologs, crossing over
Metaphase: tetrads line up at metaphase plate, random alignment
Anaphase: tetrad separation, formation at opposite poles, homologs separate with their centromeres intact
Telophase: nuclear membrane forms, two haploid daughter cells form
Meiosis II
Prophase: chromosomes condense
Metaphase: chromosomes line up single file, not pairs, on the metaphase plate
Anaphase: chromosomes split at centromere
Telophase: nuclear membrane forms and 4 total haploid cells are produced
Genetic variation
Crossing over: homologous chromosomes swap genetic material
Independent assortment: homologous chromosomes line up randomly
Random fertilization: random sperm and random egg interact
Gametogenesis
Spermatogenesis: sperm production
Oogenesis: egg cells production (¼ of them degenerate)
Fundamentals of Heredity
Traits: expressed characteristics
Gene: “chunk” of DNA that codes for a specific trait
Homologous chromosomes: two copies of a gene
Alleles: copies of chromosome may differ bc of crossing over
Homozygous/Heterozygous: identical/different
Phenotype: physical representation of genotype
Generations
Parent or P1
Filial or F1
F2
Law of dominance: one trait masks the other one
Complete: one trait completely covers the other one
Incomplete: traits are both expressed
Codominance: traits combine
Law of segregation (Mendel): each gamete gets one copy of a gene
Law of independent assortment (Mendel): traits segregate independently from one another
Locus: location of gene on chromosome
Linked genes: located on the same chromosome, loci less than 50 cM apart
Gene maps and linkage maps
Nondisjunction: inability of chromosomes to separate (ex down syndrome)
Polygenic: many genes influence one phenotype
Pleiotropic: one gene influences many phenotypes
Epistasis: one gene affects another gene
Mitochondrial and chloroplast DNA is inherited maternally
Diseases/Disorders
Genetic:
Tay-Sachs: can’t break down specific lipid in brain
Sickle cell anemia: misshapen RBCs
Color blindness
Hemophilia: lack of clotting factors
Chromosomal:
Turner: only one X chromosome
Klinefelter: XXY chromosomes
Down syndrome (trisomy 21): nondisjunction
Crosses
Sex-linked stuff
Blood type
Barr bodies: in women, two X chromosomes; different chromosomes expressed in different parts of the body, thus creating two different phenotype expressions in different places
Calculations
Pedigree/Punnett Square
Recombination stuff
Recombination rate = # of recombinable offspring/ total offspring (times 100) units: map units
Relevant Experiments
Mendel
6) Gene Expression and Regulation
Content
DNA and RNA Structure
Prokaryotic organisms typically have circular chromosomes
Plasmids = extrachromosomal circular DNA molecules
Purines (G, A) are double-ringed while pyrimidines (C, T, U) have single ring
snRNA - small nuclear RNA (bound to snRNPs - small nuclear ribonucleoproteins)
miRNA - microRNA (regulatory)
DNA Replication
Steps:
Helicase opens up the DNA at the replication fork.
Single-strand binding proteins coat the DNA around the replication fork to prevent rewinding of the DNA.
Topoisomerase works at the region ahead of the replication fork to prevent supercoiling.
Primase synthesizes RNA primers complementary to the DNA strand.
DNA polymerase III extends the primers, adding on to the 3' end, to make the bulk of the new DNA.
RNA primers are removed and replaced with DNA by DNA polymerase I.
The gaps between DNA fragments are sealed by DNA ligase.
Protein Synthesis
61 codons code for amino acids, 3 code as STOP - UAA, UAG, UGA - 64 total
Transcription Steps:
RNA polymerase binds to promoter (before gene) and separate the DNA strands
RNA polymerase fashions a complementary RNA strand from a DNA strand
Coding strand is same as RNA being made, template strand is complementary
Terminator on gene releases the RNA polymerase
RNA Processing Steps (Eukaryotes):
5’ cap and 3’ (poly-A tail, poly A polymerase) tail is added to strand (guanyl transferase)
Splicing of the RNA occurs in which introns are removed and exons are added by spliceosome
Cap/tail adds stability, splicing makes the correct sequence (“gibberish”)
Translation Steps:
Initiation complex is the set up of a ribosome around the beginning of an mRNA fragment
tRNA binds to codon, amino acid is linked to other amino acid
mRNA is shifted over one codon (5’ to 3’)
Stop codon releases mRNA
Gene Expression
Translation of mRNA to a polypeptide occurs on ribosomes in the cytoplasm as well as rough ER
Translation of the mRNA occurs during transcription in prokaryotes
Genetic info in retroviruses is an exception to normal laws: RNA to DNA is possible with reverse transcriptase, which allows the virus to integrate into the host’s DNA
Regulatory sequences = stretches of DNA that interact with regulatory proteins to control transcription
Epigenetic changes can affect expression via mods of DNA or histones
Observable cell differentiation results from the expression of genes for tissue-specific proteins
Induction of transcription factors during dev results in gene expression
Prokaryotes: operons transcribed in a single mRNA molecule, inducible system
Eukaryotes: groups of genes may be influenced by the same transcription factors to coordinate expression
Promoters = DNA sequences that RNA polymerase can latch onto to initiate
Negative regulators inhibit gene expression by binding to DNA and blocking transcription
Acetylation (add acetyl groups)- more loosely wound/ less tightly coiled/compressed
Methylation of DNA (add methyl groups) - less transcription- more tightly wound
Mutation and Genetic Variation
Disruptions in genes (mutations) change phenotypes
Mutations can be +/-/neutral based on their effects that are conferred by the protein formed - environmental context
Errors in DNA replication or repair as well as external factors such as radiation or chemical exposure cause them
Mutations are the primary source of genetic variation
Horizontal acquisition in prokaryotes - transformation (uptake of naked DNA), transduction (viral DNA transmission), conjugation (cell-cell DNA transfer), and transposition (DNA moved within/between molecules) - increase variation
Related viruses can (re)combine genetic material in the same host cell
Types of mutations: frameshift, deletion, insertion
Genetic Engineering
Electrophoresis separates molecules by size and charge
PCR magnifies DNA fragments
Bacterial transformation introduces DNA into bacterial cells
Operons
Almost always prokaryotic
Promoter region has operator in it
Structural genes follow promoter
Terminator ends operon
Regulatory protein is active repressor
Active repressor can be inactivated
Enhancer: remote gene that require activators
RNAi: interference with miRNA
Anabolic pathways are normally on and catabolic pathways are normally off
Calculations
Transformation efficiency (colonies/DNA)
Numbers of base pairs (fragment lengths)
Cutting enzymes in a plasmid or something (finding the lengths of each section)
Labs
Gel Electrophoresis Lab
Phosphates in DNA make it negative (even though it’s an acid!), so it moves to positive terminal on the board
Smaller DNA is quicc, compare it to a standard to calculate approx. lengths
Bacterial Transformation Lab
Purpose of sugar: arabinose is a promoter which controls the GFP in transformed cells, turns it on, also green under UV
Purpose of flipping upside down: condensation forms but doesn’t drip down
Purpose of heat shock: increases bacterial uptake of foreign DNA
Plasmids have GFP (green fluorescent protein) and ampicillin resistance genes
Calcium solution puts holes in bacteria to allow for uptake of plasmids
PCR Lab
DNA + primers + nucleotides + DNA polymerase in a specialized PCR tube in a thermal cycler
Primers bind to DNA before it can repair itself, DNA polymerase binds to the primers and begins replication
After 30 cycles, there are billions of target sequences
Relevant Experiments
Avery: harmful + harmless bacteria in mice, experimented with proteins vs DNA of bacteria
Griffith: Avery’s w/o DNA vs protein
Hershey and Chase: radioactively labeled DNA and protein
Melson and Stahl: isotopic nitrogen in bacteria, looked for cons/semi/dispersive DNA
Beadle and Tatum: changed medium’s amino acid components to find that a metabolic pathway was responsible for turning specific proteins into other proteins, “one gene one enzyme”
Nirenberg: discovered codon table
7) Natural Selection
Scientific Theory: no refuting evidence (observation + experimentation), time, explain a brand/extensive range of phenomena
Theory of Natural Selection
Definition
Not all offspring (in a population) will survive
Variation among individuals in a population
Some variations were more favourable than others in a particular environment
Those with more favourable variations were more likely to survive and reproduce.
These favourable variations were passed on and increased in frequency over time.
Types of Selection:
Directional selection: one phenotype favored at one of the extremes of the normal distribution
”Weeds out” one phenotype
Ony can happen if a favored allele is already present
Stabilizing Selection: Organisms within a population are eliminated with extreme traits
Favors “average” or medium traits
Ex. big head causes a difficult delivery; small had causes health deficits
Disruptive Selection: favors both extremes and selects against common traits
Ex. sexual selection (seems like directional but it’s not because it only affects one sex, if graph is only males then directional)
Competition for limited resources results in differential survival, favourable phenotypes are more likely to survive and produce more offspring, thus passing traits to subsequent generations.
Biotic and abiotic environments can be more or less stable/fluctuating, and this affects the rate and direction of evolution
Convergent evolution occurs when similar selective pressures result in similar phenotypic adaptations in different populations or species.
Divergent evolution: groups from common ancestor evolve, homology
Different genetic variations can be selected in each generation.
Environments change and apply selective pressures to populations.
Evolutionary fitness is measured by reproductive success.
Natural selection acts on phenotypic variations in populations.
Some phenotypic variations significantly increase or decrease the fitness of the organism in particular environments.
Through artificial selection, humans affect variation in other species.
Humans choose to cause artificial selection with specific traits, accidental selection caused by humans is not artificial
Random occurrences
Mutation
Genetic drift - change in existing allele frequency
Migration
Reduction of genetic variation within a given population can increase the differences between populations of the same species.
Conditions for a population or an allele to be in Hardy-Weinberg equilibrium are
Large population size
Absence of migration
No net mutations
Random mating
Absence of selection
Changes in allele frequencies provide evidence for the occurrence of evolution in a population.
Small populations are more susceptible to random environmental impact than large populations.
Gene flow: transference of genes/alleles between populations
Speciation: one species splits off into multiple species
Sympatric (living together i.e. disruption) Allopatric (physically separate, i.e. founder effect) Parapatric (habitats overlapping)
Polyploidy (autopolyploidy), sexual selection
Species: group of populations whose members can interbreed and produce healthy, fertile offspring but can’t breed with other species (ex. a horse and donkey can produce a mule but a mule is nonviable, so it doesn’t qualify)
Morphological definition: body shape and structural characteristics define a species
Ecological species definition: way populations interact with their environments define a species
Phylogenetic species definition: smallest group that shares a common ancestor is a species
Prezygotic barriers: barriers to reproduction before zygote is formed
Geographical error: two organisms are in different areas
Behavioural error (i.e. mating rituals aren’t the same)
Mechanical error: “the pieces don’t fit together”
Temporal error (i.e. one organism comes out at night while the other comes out in the day)
Zygotic/Gametic isolation: sperm and egg don’t physically meet
Postzygotic barriers: barriers to reproduction after zygote is formed
Hybrid viability: developmental errors of offspring
Hybrid fertility: organism is sterilized
Hybrid breakdown: offspring over generations aren’t healthy
Hybrid zone: region in which members of different species meet and mate
Reinforcement: hybrids less fit than parents, die off, strength prezygotic barriers
Fusion: two species may merge into one population
Stability: stable hybrid zones mean hybrids are more fit than parents, thus creating a stable population, but can be selected against in hybrid zones as well
Punctuated equilibria: long periods of no or little change evolutionarily punctuated by short periods of large change, gradualism is just slow evolution
Evidence of evolution
Paleontology (Fossils)
Comparative Anatomy
Embryology: embryos look the same as they grow
Biogeography: distribution of flora and fauna in the environment (pangea!)
Biochemical: DNA and proteins and stuff, also glycolysis
Phylogenetic trees
Monophyletic: common ancestor and all descendants
Polyphyletic: descendants with different ancestors
Paraphyletic: leaving specifies out of group
Out group: basal taxon, doesn’t have traits others do
Cline: graded variation within species (i.e. different stem heights based on altitude)
Anagenesis: one species turning into another species
Cladogenesis: one species turning into multiple species
Taxon: classification/grouping
Clade: group of species with common ancestor
Horizontal gene transfer: genes thrown between bacteria
Shared derived characters: unique to specific group
Shared primitive/ancestral characters: not unique to a specific group but is shared within group
Origins of life
Stages
Inorganic formation of organic monomers (miller-urey experiment)
Inorganic formation of organic polymers (catalytic surfaces like hot rock or sand)
Protobionts and compartmentalization (liposomes, micelles)
DNA evolution (RNA functions as enzyme)
Shared evolutionary characteristics across all domains
Membranes
Cell comm.
Gene to protein
DNA
Proteins
Extant = not extinct
Highly conserved genes = low rates of mutation in history due to criticalness (like electron transport chain)
Molecular clock: dating evolution using DNA evidence
Extinction causes niches for species to fill
Eukaryotes all have common ancestor (shown by membrane-bound organelles, linear chromosomes, and introns)
Calculations
Hardy-Weinberg
p + q = 1
p^2 + 2pq +q^2 = 1
Chi Squared
Labs
Artificial Selection Lab
Trichrome trait hairs
Anthocyanin for second trait (purple stems)
Function of the purple pigment?
Function of trichome hairs?
BLAST Lab
Putting nucleotides into a database outputs similar genes
Relevant Experiments
Darwin
Lamarck
Miller-Urey
Slapped some water, methane, ammonia, and hydrogen is some flasks and simulated early earth with heat and stuff and it made some amino acids.
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Some dope project phoenix approved content for y'all: First 40,000 characters of the LSD wikipedia. Enjoy!
No one likes pictures anyway. Now you can only post about what a badass you are taking 50 tabs at once or other great text based content like the LSD wikipedia page(made sure to remove the music and art section): From Wikipedia, the free encyclopedia (Redirected from Lsd)Jump to navigationJump to search"LSD" redirects here. For other uses, see LSD (disambiguation).Lysergic acid diethylamide (LSD) INN: Lysergide📷2D structural formula and 3D models of LSDClinical dataPronunciation/daɪ eθəl ˈæmaɪd/, /æmɪd/, or /eɪmaɪd/[3][4][5]Other namesLSD, LSD-25, Acid, Delysid, othersAHFS/Drugs.comReferencePregnancy category - US: C (Risk not ruled out) Dependence liabilityLow[2]Addiction liabilityLow-rare[1]Routes of administrationBy mouth, under the tongue, intravenousDrug classHallucinogen (serotonergic psychedelic)ATC code - None Legal statusLegal status - AU: S9 (Prohibited) - CA: Schedule III - DE: Anlage I (Authorized scientific use only) - NZ: Class A - UK: Class A - US: Schedule I - UN: Psychotropic Schedule I Pharmacokinetic dataBioavailability71%[6]Protein bindingUnknown[7]MetabolismLiver (CYP450)[6]Metabolites2-Oxo-3-hydroxy-LSD[6]Onset of action30–40 minutes[8]Elimination half-life3.6 hours[6][9]Duration of action8–12 hours[10]ExcretionKidneys[6][9]IdentifiersIUPAC name[show]CAS Number - 50-37-3 📷 PubChem CID - 5761 IUPHABPS - 17 DrugBank - DB04829 📷 ChemSpider - 5558 📷 UNII - 8NA5SWF92O ChEBI - CHEBI:6605 📷 ChEMBL - ChEMBL263881 📷 PDB ligand - 7LD (PDBe, RCSB PDB) CompTox Dashboard (EPA) - DTXSID1023231 📷 ECHA InfoCard100.000.031 📷Chemical and physical dataFormulaC20H25N3OMolar mass323.440 g·mol−13D model (JSmol) - Interactive image Melting point80 to 85 °C (176 to 185 °F)SMILES[show]InChI[show] (verify) Lysergic acid diethylamide (LSD),[a] also known as acid, is a hallucinogenic drug.[11] Effects typically include altered thoughts, feelings, and awareness of one's surroundings.[11] Many users see or hear things that do not exist.[12] Dilated pupils, increased blood pressure, and increased body temperature are typical.[13] Effects typically begin within half an hour and can last for up to 12 hours.[13] It is used mainly as a recreational drug and for spiritual reasons.[13][14] LSD does not appear to be addictive, although tolerance may occur with use of increasing doses.[11][15] Adverse psychiatric reactions are possible, such as anxiety, paranoia, and delusions.[7] Distressing flashbacks might occur in spite of no further use, a condition called hallucinogen persisting perception disorder.[16][17] Death is very rare as a result of LSD, though it occasionally occurs in accidents.[13] The effects of LSD are believed to occur as a result of alterations in the serotonin system.[13] As little as 20 micrograms can produce an effect.[13] In pure form, LSD is clear or white in color, has no smell, and is crystalline.[11] It breaks down with exposure to ultraviolet light.[13] About 10 percent of people in the United States have used LSD at some point in their lives as of 2017, while 0.7 percent have used it in the last year.[12] It was most popular in the 1960s to 1980s.[13] LSD is typically either swallowed or held under the tongue.[11] It is most often sold on blotter paper and less commonly as tablets or in gelatin squares.[13] There is no known treatment for addiction, if it occurs.[16] LSD was first made by Albert Hofmann in 1938 from lysergic acid, a chemical from the fungus ergot.[13][16] Hofmann discovered its hallucinogenic properties in 1943.[18] In the 1950s, the Central Intelligence Agency (CIA) believed that the drug might be useful for mind control, so they tested it on people, some without their knowledge, in a program called MKUltra.[19] LSD was sold as a medication for research purposes under the trade-name Delysid in the 1950s and 1960s.[13][20] It was listed as a schedule 1 controlled substance by the United Nations in 1971.[13] It currently has no approved medical use.[13] In Europe, as of 2011, the typical cost of a dose was between €4.50 and €25.[13] Contents - 1Uses - 1.1Recreational - 1.2Spiritual - 1.3Medical - 2Effects - 2.1Physical - 2.2Psychological - 2.3Sensory - 3Adverse effects - 3.1Mental disorders - 3.2Suggestibility - 3.3Flashbacks - 3.4Cancer and pregnancy - 3.5Tolerance - 3.6Addiction - 4Overdose - 5Pharmacology - 5.1Pharmacodynamics - 5.2Pharmacokinetics - 6Chemistry - 6.1Synthesis - 6.2Dosage - 6.3Reactivity and degradation - 6.4Detection - 7History - 8Society and culture - 8.1Counterculture - 8.2Music and art - 8.3Legal status - 8.4Economics - 9Research - 9.1Psychedelic therapy - 9.2Other uses - 10Notable individuals - 11See also - 12Notes - 13References - 14Further reading - 15External links - 15.1Documentaries Uses Recreational LSD is commonly used as a recreational drug.[21] Spiritual LSD is considered an entheogen because it can catalyze intense spiritual experiences, during which users may feel they have come into contact with a greater spiritual or cosmic order. Users sometimes report out of body experiences. In 1966, Timothy Leary established the League for Spiritual Discovery with LSD as its sacrament.[22][23] Stanislav Grof has written that religious and mystical experiences observed during LSD sessions appear to be phenomenologically indistinguishable from similar descriptions in the sacred scriptures of the great religions of the world and the texts of ancient civilizations.[24] Medical See also: Lysergic acid diethylamide § Research LSD currently has no approved uses in medicine.[25][26] A meta analysis concluded that a single dose was effective at reducing alcohol consumption in alcoholism.[27] LSD has also been studied in depression, anxiety, and drug dependence, with positive preliminary results.[28] Effects 📷Some symptoms reported for LSD[29][30] Physical LSD can cause pupil dilation, reduced appetite, and wakefulness. Other physical reactions to LSD are highly variable and nonspecific, some of which may be secondary to the psychological effects of LSD. Among the reported symptoms are numbness, weakness, nausea, hypothermia or hyperthermia, elevated blood sugar, goose bumps, heart rate increase, jaw clenching, perspiration, saliva production, mucus production, hyperreflexia, and tremors. Psychological The most common immediate psychological effects of LSD are visual hallucinations and illusions (colloquially known as "trips"), which can vary depending on how much is used and how the brain responds. Trips usually start within 20–30 minutes of taking LSD by mouth (less if snorted or taken intravenously), peak three to four hours after ingestion, and last up to 12 hours. Negative experiences, referred to as "bad trips," produce intense negative emotions, such as irrational fears and anxiety, panic attacks, paranoia, rapid mood swings, hopelessness, intrusive thoughts of harming others, and suicidal ideation. It is impossible to predict when a bad trip will occur.[31][32] Good trips are stimulating and pleasurable, and typically involve feeling as if one is floating, feeling disconnected from reality, feelings of joy or euphoria (sometimes called a "rush"), decreased inhibitions, and the belief that one has extreme mental clarity or superpowers.[31] "Reliable reports of bizarre crimes of violence, homicides, suicides and self-mutilations directly associated with the use of hallucinogens are uncommon, although unsubstantiated rumors are abundant."[33] Sensory Some sensory effects may include an experience of radiant colors, objects and surfaces appearing to ripple or "breathe," colored patterns behind the closed eyelids (eidetic imagery), an altered sense of time (time seems to be stretching, repeating itself, changing speed or stopping), crawling geometric patterns overlaying walls and other objects, and morphing objects.[34] Some users, including Albert Hofmann, report a strong metallic taste for the duration of the effects.[35] LSD causes an animated sensory experience of senses, emotions, memories, time, and awareness for 6 to 14 hours, depending on dosage and tolerance. Generally beginning within 30 to 90 minutes after ingestion, the user may experience anything from subtle changes in perception to overwhelming cognitive shifts. Changes in auditory and visual perception are typical.[34][36] Visual effects include the illusion of movement of static surfaces ("walls breathing"), after image-like trails of moving objects ("tracers"), the appearance of moving colored geometric patterns (especially with closed eyes), an intensification of colors and brightness ("sparkling"), new textures on objects, blurred vision, and shape suggestibility. Some users report that the inanimate world appears to animate in an inexplicable way; for instance, objects that are static in three dimensions can seem to be moving relative to one or more additional spatial dimensions.[37] Many of the basic visual effects resemble the phosphenes seen after applying pressure to the eye and have also been studied under the name "form constants." The auditory effects of LSD may include echo-like distortions of sounds, changes in ability to discern concurrent auditory stimuli, and a general intensification of the experience of music. Higher doses often cause intense and fundamental distortions of sensory perception such as synaesthesia, the experience of additional spatial or temporal dimensions, and temporary dissociation. Adverse effects 📷Addiction experts in psychiatry, chemistry, pharmacology, forensic science, epidemiology, and the police and legal services engaged in delphic analysis regarding 20 popular recreational drugs. LSD was ranked 14th in dependence, 15th in physical harm, and 13th in social harm.[38] Of the 20 drugs ranked according to individual and societal harm by David Nutt, LSD was third to last, approximately 1/10th as harmful as alcohol. The most significant adverse effect was impairment of mental functioning while intoxicated.[39] Mental disorders LSD may trigger panic attacks or feelings of extreme anxiety, known familiarly as a "bad trip." Review studies suggest that LSD likely plays a role in precipitating the onset of acute psychosis in previously healthy individuals with an increased likelihood in individuals who have a family history of schizophrenia.[7][40] There is evidence that people with severe mental illnesses like schizophrenia have a higher likelihood of experiencing adverse effects from taking LSD.[40] Suggestibility While publicly available documents indicate that the CIA and Department of Defense have discontinued research into the use of LSD as a means of mind control,[41] research from the 1960s suggests that both mentally ill and healthy people are more suggestible while under its influence.[42][43][non-primary source needed] Flashbacks "Flashbacks" are a reported psychological phenomenon in which an individual experiences an episode of some of LSD's subjective effects after the drug has worn off, "persisting for months or years after hallucinogen use."[44] A diagnosable condition called hallucinogen persisting perception disorder has been defined to describe intermittent or chronic flashbacks that cause distress or impairment in life and work, and are caused only by prior hallucinogen use and not some other condition.[17] Cancer and pregnancy The mutagenic potential of LSD is unclear. Overall, the evidence seems to point to limited or no effect at commonly used doses.[45] Studies showed no evidence of teratogenic or mutagenic effects.[7] Tolerance Tolerance to LSD builds up with consistent use[46] and cross-tolerance has been demonstrated between LSD, mescaline[47] and psilocybin.[48] Researchers believe that tolerance returns to baseline after two weeks of being drug free.[49] Addiction The NIH comments that LSD is addictive,[16] while other sources state it is not.[15][50] A 2009 textbook states that it "rarely produce[s] compulsive use."[1] A 2006 review states it is readily abused but does not result in addiction.[15] Overdose As of 2008 there were no documented fatalities attributed directly to an LSD overdose.[7] Despite this several behavioral fatalities and suicides have occurred due to LSD.[51][52] Eight individuals who accidentally consumed very high amounts by mistaking LSD for cocaine developed comatose states, hyperthermia, vomiting, gastric bleeding, and respiratory problems—however, all survived with supportive care.[7] Reassurance in a calm, safe environment is beneficial. Agitation can be safely addressed with benzodiazepines such as lorazepam or diazepam. Neuroleptics such as haloperidol are recommended against because they may have adverse effects. LSD is rapidly absorbed, so activated charcoal and emptying of the stomach is of little benefit, unless done within 30–60 minutes of ingesting an overdose of LSD. Sedation or physical restraint is rarely required, and excessive restraint may cause complications such as hyperthermia (over-heating) or rhabdomyolysis.[53] Research suggests that massive doses are not lethal, but do typically require supportive care, which may include endotracheal intubation or respiratory support.[53] It is recommended that high blood pressure, tachycardia (rapid heart-beat), and hyperthermia, if present, are treated symptomatically, and that low blood pressure is treated initially with fluids and then with pressors if necessary. Intravenous administration of anticoagulants, vasodilators, and sympatholytics may be useful with massive doses.[53] Pharmacology Pharmacodynamics 📷Binding affinities of LSD for various receptors. The lower the dissociation constant (Ki), the more strongly LSD binds to that receptor (i.e. with higher affinity). The horizontal line represents an approximate value for human plasma concentrations of LSD, and hence, receptor affinities that are above the line are unlikely to be involved in LSD's effect. Data averaged from data from the Ki Database Most serotonergic psychedelics are not significantly dopaminergic, and LSD is therefore atypical in this regard. The agonism of the D2 receptor by LSD may contribute to its psychoactive effects in humans.[54][55] LSD binds to most serotonin receptor subtypes except for the 5-HT3 and 5-HT4 receptors. However, most of these receptors are affected at too low affinity to be sufficiently activated by the brain concentration of approximately 10–20 nM.[50] In humans, recreational doses of LSD can affect 5-HT1A (Ki=1.1nM), 5-HT2A (Ki=2.9nM), 5-HT2B (Ki=4.9nM), 5-HT2C (Ki=23nM), 5-HT5A (Ki=9nM [in cloned rat tissues]), and 5-HT6 receptors (Ki=2.3nM).[56][57] 5-HT5B receptors, which are not present in humans, also have a high affinity for LSD.[58] The psychedelic effects of LSD are attributed to cross-activation of 5-HT2A receptor heteromers.[59] Many but not all 5-HT2A agonists are psychedelics and 5-HT2A antagonists block the psychedelic activity of LSD. LSD exhibits functional selectivity at the 5-HT2A and 5HT2C receptors in that it activates the signal transduction enzyme phospholipase A2 instead of activating the enzyme phospholipase C as the endogenous ligand serotonin does.[60] Exactly how LSD produces its effects is unknown, but it is thought that it works by increasing glutamate release in the cerebral cortex[50] and therefore excitation in this area, specifically in layers IV and V.[61] LSD, like many other drugs of recreational use, has been shown to activate DARPP-32-related pathways.[62] The drug enhances dopamine D2 receptor protomer recognition and signaling of D2–5-HT2A receptor complexes,[63] which may contribute to its psychotic effects.[63] LSD has been shown to have low affinity for H1 receptors, displaying antihistamine effects.[64][65][66] The crystal structure of LSD bound in its active state to a serotonin receptor, specifically the 5-HT2B receptor, has been elucidated for the first time in 2017.[67][68][69] The LSD-bound 5-HT2B receptor is regarded as an excellent model system for the 5-HT2A receptor and the structure of the LSD-bound 5-HT2B receptor was used in the study as a template to determine the structural features necessary for the activity of LSD at the 5-HT2A receptor.[67][68][69] The diethylamide moiety of LSD was found to be a key component for its activity, which is in accordance with the fact that the related lysergamide lysergic acid amide (LSA) is far less hallucinogenic in comparison.[69] LSD was found to stay bound to both the 5-HT2A and 5-HT2B receptors for an exceptionally long amount of time, which may be responsible for its long duration of action in spite of its relatively short terminal half-life.[67][68][69] The extracellular loop 2 leucine 209 residue of the 5-HT2B receptor forms a 'lid' over LSD that appears to trap it in the receptor, and this was implicated in the potency and functional selectivity of LSD and its very slow dissociation rate from the 5-HT2 receptors.[67][68][69] Pharmacokinetics The effects of LSD normally last between 6 and 12 hours depending on dosage, tolerance, body weight, and age.[70] The Sandoz prospectus for "Delysid" warned: "intermittent disturbances of affect may occasionally persist for several days."[71] Aghajanian and Bing (1964) found LSD had an elimination half-life of only 175 minutes (about 3 hours).[56] However, using more accurate techniques, Papac and Foltz (1990) reported that 1 µg/kg oral LSD given to a single male volunteer had an apparent plasma half-life of 5.1 hours, with a peak plasma concentration of 5 ng/mL at 3 hours post-dose.[72] The pharmacokinetics of LSD were not properly determined until 2015, which is not surprising for a drug with the kind of low-μg potency that LSD possesses.[9][6] In a sample of 16 healthy subjects, a single mid-range 200 μg oral dose of LSD was found to produce mean maximal concentrations of 4.5 ng/mL at a median of 1.5 hours (range 0.5–4 hours) post-administration.[9][6] After attainment of peak levels, concentrations of LSD decreased following first-order kinetics with a terminal half-life of 3.6 hours for up to 12 hours and then with slower elimination with a terminal half-life of 8.9 hours thereafter.[9][6] The effects of the dose of LSD given lasted for up to 12 hours and were closely correlated with the concentrations of LSD present in circulation over time, with no acute tolerance observed.[9][6] Only 1% of the drug was eliminated in urine unchanged whereas 13% was eliminated as the major metabolite 2-oxo-3-hydroxy-LSD (O-H-LSD) within 24 hours.[9][6] O-H-LSD is formed by cytochrome P450 enzymes, although the specific enzymes involved are unknown, and it does not appear to be known whether O-H-LSD is pharmacologically active or not.[9][6] The oral bioavailability of LSD was crudely estimated as approximately 71% using previous data on intravenous administration of LSD.[9][6] The sample was equally divided between male and female subjects and there were no significant sex differences observed in the pharmacokinetics of LSD.[9][6] Chemistry 📷The four possible stereoisomers of LSD. Only (+)-LSD is psychoactive. LSD is a chiral compound with two stereocenters at the carbon atoms C-5 and C-8, so that theoretically four different optical isomers of LSD could exist. LSD, also called (+)-D-LSD,[citation needed] has the absolute configuration (5R,8R). The C-5 isomers of lysergamides do not exist in nature and are not formed during the synthesis from d-lysergic acid. Retrosynthetically, the C-5 stereocenter could be analysed as having the same configuration of the alpha carbon of the naturally occurring amino acid L-tryptophan, the precursor to all biosynthetic ergoline compounds. However, LSD and iso-LSD, the two C-8 isomers, rapidly interconvert in the presence of bases, as the alpha proton is acidic and can be deprotonated and reprotonated. Non-psychoactive iso-LSD which has formed during the synthesis can be separated by chromatography and can be isomerized to LSD. Pure salts of LSD are triboluminescent, emitting small flashes of white light when shaken in the dark.[70] LSD is strongly fluorescent and will glow bluish-white under UV light. Synthesis LSD is an ergoline derivative. It is commonly synthesized by reacting diethylamine with an activated form of lysergic acid. Activating reagents include phosphoryl chloride[73] and peptide coupling reagents.[74] Lysergic acid is made by alkaline hydrolysis of lysergamides like ergotamine, a substance usually derived from the ergot fungus on agar plate; or, theoretically possible, but impractical and uncommon, from ergine (lysergic acid amide, LSA) extracted from morning glory seeds.[75] Lysergic acid can also be produced synthetically, eliminating the need for ergotamines.[76][77] Dosage 📷White on White blotters (WoW) for sublingual administration A single dose of LSD may be between 40 and 500 micrograms—an amount roughly equal to one-tenth the mass of a grain of sand. Threshold effects can be felt with as little as 25 micrograms of LSD.[78][79] Dosages of LSD are measured in micrograms (µg), or millionths of a gram. By comparison, dosages of most drugs, both recreational and medicinal, are measured in milligrams (mg), or thousandths of a gram. For example, an active dose of mescaline, roughly 0.2 to 0.5 g, has effects comparable to 100 µg or less of LSD.[71] In the mid-1960s, the most important black market LSD manufacturer (Owsley Stanley) distributed acid at a standard concentration of 270 µg,[80] while street samples of the 1970s contained 30 to 300 µg. By the 1980s, the amount had reduced to between 100 and 125 µg, dropping more in the 1990s to the 20–80 µg range,[81] and even more in the 2000s (decade).[80][82] Reactivity and degradation "LSD," writes the chemist Alexander Shulgin, "is an unusually fragile molecule ... As a salt, in water, cold, and free from air and light exposure, it is stable indefinitely."[70] LSD has two labile protons at the tertiary stereogenic C5 and C8 positions, rendering these centres prone to epimerisation. The C8 proton is more labile due to the electron-withdrawing carboxamide attachment, but removal of the chiral proton at the C5 position (which was once also an alpha proton of the parent molecule tryptophan) is assisted by the inductively withdrawing nitrogen and pi electron delocalisation with the indole ring.[citation needed] LSD also has enamine-type reactivity because of the electron-donating effects of the indole ring. Because of this, chlorine destroys LSD molecules on contact; even though chlorinated tap water contains only a slight amount of chlorine, the small quantity of compound typical to an LSD solution will likely be eliminated when dissolved in tap water.[70] The double bond between the 8-position and the aromatic ring, being conjugated with the indole ring, is susceptible to nucleophilic attacks by water or alcohol, especially in the presence of light. LSD often converts to "lumi-LSD," which is inactive in human beings.[70] A controlled study was undertaken to determine the stability of LSD in pooled urine samples.[83] The concentrations of LSD in urine samples were followed over time at various temperatures, in different types of storage containers, at various exposures to different wavelengths of light, and at varying pH values. These studies demonstrated no significant loss in LSD concentration at 25 °C for up to four weeks. After four weeks of incubation, a 30% loss in LSD concentration at 37 °C and up to a 40% at 45 °C were observed. Urine fortified with LSD and stored in amber glass or nontransparent polyethylene containers showed no change in concentration under any light conditions. Stability of LSD in transparent containers under light was dependent on the distance between the light source and the samples, the wavelength of light, exposure time, and the intensity of light. After prolonged exposure to heat in alkaline pH conditions, 10 to 15% of the parent LSD epimerized to iso-LSD. Under acidic conditions, less than 5% of the LSD was converted to iso-LSD. It was also demonstrated that trace amounts of metal ions in buffer or urine could catalyze the decomposition of LSD and that this process can be avoided by the addition of EDTA. Detection LSD may be quantified in urine as part of a drug abuse testing program, in plasma or serum to confirm a diagnosis of poisoning in hospitalized victims or in whole blood to assist in a forensic investigation of a traffic or other criminal violation or a case of sudden death. Both the parent drug and its major metabolite are unstable in biofluids when exposed to light, heat or alkaline conditions and therefore specimens are protected from light, stored at the lowest possible temperature and analyzed quickly to minimize losses.[84] The apparent plasma half life of LSD is considered to be around 5.1 hours with peak plasma concentrations occurring 3 hours after administration.[85] LSD can be detected using an Ehrlich's reagent and a Hofmann's reagent. History ... affected by a remarkable restlessness, combined with a slight dizziness. At home I lay down and sank into a not unpleasant intoxicated-like condition, characterized by an extremely stimulated imagination. In a dreamlike state, with eyes closed (I found the daylight to be unpleasantly glaring), I perceived an uninterrupted stream of fantastic pictures, extraordinary shapes with intense, kaleidoscopic play of colors. After some two hours this condition faded away. —Albert Hofmann, on his first experience with LSD[86] Main article: History of lysergic acid diethylamide LSD was first synthesized on November 16, 1938[87] by Swiss chemist Albert Hofmann at the Sandoz Laboratories in Basel, Switzerland as part of a large research program searching for medically useful ergot alkaloid derivatives. LSD's psychedelic properties were discovered 5 years later when Hofmann himself accidentally ingested an unknown quantity of the chemical.[88] The first intentional ingestion of LSD occurred on April 19, 1943,[89] when Hofmann ingested 250 µg of LSD. He said this would be a threshold dose based on the dosages of other ergot alkaloids. Hofmann found the effects to be much stronger than he anticipated.[90] Sandoz Laboratories introduced LSD as a psychiatric drug in 1947 and marketed LSD as a psychiatric panacea, hailing it "as a cure for everything from schizophrenia to criminal behavior, 'sexual perversions,' and alcoholism."[91] The abbreviation "LSD" is from the German "Lysergsäurediethylamid".[92] 📷Albert Hofmann in 2006 Beginning in the 1950s, the US Central Intelligence Agency (CIA) began a research program code named Project MKUltra. The CIA introduced LSD to the United States, purchasing the entire world's supply for $240,000 and propagating the LSD, through CIA front organizations to American hospitals, clinics, prisons and research centers.[93] Experiments included administering LSD to CIA employees, military personnel, doctors, other government agents, prostitutes, mentally ill patients, and members of the general public in order to study their reactions, usually without the subjects' knowledge. The project was revealed in the US congressional Rockefeller Commission report in 1975. In 1963, the Sandoz patents expired on LSD.[81] Several figures, including Aldous Huxley, Timothy Leary, and Al Hubbard, began to advocate the consumption of LSD. LSD became central to the counterculture of the 1960s.[94] In the early 1960s the use of LSD and other hallucinogens was advocated by new proponents of consciousness expansion such as Leary, Huxley, Alan Watts and Arthur Koestler,[95][96] and according to L. R. Veysey they profoundly influenced the thinking of the new generation of youth.[97] On October 24, 1968, possession of LSD was made illegal in the United States.[98] The last FDA approved study of LSD in patients ended in 1980, while a study in healthy volunteers was made in the late 1980s. Legally approved and regulated psychiatric use of LSD continued in Switzerland until 1993.[99] Society and culture Counterculture 📷This section needs additional citations for verification. Please help improve this article by adding citations to reliable sources. Unsourced material may be challenged and removed. Find sources: "Lysergic acid diethylamide" – news · newspapers · books · scholar · JSTOR (March 2016) (Learn how and when to remove this template message)📷Psychedelic art attempts to capture the visions experienced on a psychedelic trip By the mid-1960s, the youth countercultures in California, particularly in San Francisco, had adopted the use of hallucinogenic drugs, with the first major underground LSD factory established by Owsley Stanley.[100] From 1964, the Merry Pranksters, a loose group that developed around novelist Ken Kesey, sponsored the Acid Tests, a series of events primarily staged in or near San Francisco, involving the taking of LSD (supplied by Stanley), accompanied by light shows, film projection and discordant, improvised music known as the psychedelic symphony.[101][102] The Pranksters helped popularize LSD use, through their road trips across America in a psychedelically-decorated converted school bus, which involved distributing the drug and meeting with major figures of the beat movement, and through publications about their activities such as Tom Wolfe's The Electric Kool-Aid Acid Test (1968).[103] In San Francisco's Haight-Ashbury neighborhood, brothers Ron and Jay Thelin opened the Psychedelic Shop in January 1966. The Thelins' store is regarded as the first ever head shop. The Thelins opened the store to promote safe use of LSD, which was then still legal in California. The Psychedelic Shop helped to further popularize LSD in the Haight and to make the neighborhood the unofficial capital of the hippie counterculture in the United States. Ron Thelin was also involved in organizing the Love Pageant rally, a protest held in Golden Gate park to protest California's newly adopted ban on LSD in October 1966. At the rally, hundreds of attendees took acid in unison. Although the Psychedelic Shop closed after barely a year-and-a-half in business, its role in popularizing LSD was considerable.[104] 📷"Lysergic Acid Diethylamide"📷MENU0:00by Lambert P. Lambert and the Gorgettes, from the album Abbra Cadaver, 1967Problems playing this file? See media help. A similar and connected nexus of LSD use in the creative arts developed around the same time in London. A key figure in this phenomenon in the UK was British academic Michael Hollingshead, who first tried LSD in America in 1961 while he was the Executive Secretary for the Institute of British-American Cultural Exchange. After being given a large quantity of pure Sandoz LSD (which was still legal at the time) and experiencing his first "trip," Hollingshead contacted Aldous Huxley, who suggested that he get in touch with Harvard academic Timothy Leary, and over the next few years, in concert with Leary and Richard Alpert, Hollingshead played a major role in their famous LSD research at Millbrook before moving to New York City, where he conducted his own LSD experiments. In 1965 Hollingshead returned to the UK and founded the World Psychedelic Center in Chelsea, London.
CHEM 163: General Chemistry III Bellevue College Solution: Basic Net ionic equation: HC 2 H 3 O 2(aq) + NaOH (aq) → NaC 2 H 3 O 2(aq) + H 2 O (l) Explanation for pH of the salt solution: Because of weak acid HC 2 H 3 O 2 and strong base NaOH the solution will be basic meaning the pH would be above 7 2.) Part II. Discuss why the pH of your buffer changes when you change the concentration of ... A buffer is a solution of weak acid and conjugate base or weak base and conjugate acid used to resist pH change with added solute. ... In chemistry, pH is a measure of the hydrogen ion (H +) concentration in a solution. The pH of a buffer can be calculated from the concentrations of the various components of the reaction. ... meaning they are ... A 0.10 M solution of acetic acid is only about 1.3% ionized, meaning that the equilibrium strongly favors the reactants. Weak acids, like strong acids, ionize to yield the H + ion and a conjugate base. Because HCl is a strong acid, its conjugate base (Cl − ) is extremely weak. Define conjugate. conjugate synonyms, conjugate pronunciation, conjugate translation, English dictionary definition of conjugate. ... Chemistry A chemical compound that has been formed by the joining of two or more compounds. ... solution - a homogeneous mixture of two or more substances; frequently ... The acid loses a proton to become its conjugate base A-as the base B accepts a proton to become its conjugate acid HB +. (3) Conjugation is the overlap of p-orbitals across a σ bond ( sigma bond ). In transition metals, d-orbitals may overlap. Conjugate is what you do to a word to make it agree with other words in a sentence. ... to make it agree with the subject. You might conjugate other words to make them agree in number, gender, or tense. In chemistry, conjugate means "to join together." It can also be an adjective, meaning "joined," or "joined in pairs," like the conjugate leaf ... Conjugate Acid Definition . Conjugate acids and bases are Bronsted-Lowry acid and base pairs, determined by which species gains or loses a proton.When a base dissolves in water, the species that gains a hydrogen (proton) is the base's conjugate acid. Conjugate solution definition, a system of liquids, each partially miscible in the other, existing with a common interface, consisting of a saturated solution of one in the other. See more. Define conjugated. conjugated synonyms, conjugated pronunciation, conjugated translation, English dictionary definition of conjugated. adj. Chemistry 1. Linked with another compound, or composed of two linked compounds: conjugated estrogens. A conjugate acid-base pair is a pair of substances that differ by one H+ ion. For example, HCl and Cl− are a conjugate pair where HCl is the acid and Cl− is the base. Similarly, NH3 and NH4+ are a conjugate pair where NH4+ is the acid and NH3 is the base. Note that the acid in each pair has more H atoms and the higher charge.
High school and University-Level Chemistry Help. Ask me questions, I will help you figure it out. http://leah4sci.com/acidbase presents: Introduction to Acids and Bases in Organic Chemistry including Arrhenius, Bronsted-Lowry and Lewis Explanations.Need h... Strong acids almost completely dissociate in water. They produce a weak conjugate base. Weak in this case means that the base produced rarely reacts with t... For PDF Notes and best Assignments visit @ http://physicswallahalakhpandey.com/Live Classes, Video Lectures, Test Series, Lecturewise notes, topicwise DPP, ... For more chemistry science videos for, please visit https://www.makemegenius.com/chemistry-video-lessons-for-kids.phpUnderstanding Solution and its different... This chemistry video provides a basic introduction into solubility and how compounds dissolve in water. It discusses how water separates sodium cations from... What is meaning + Definition of Solution + Homogeneous +Binary + solute +Solvent ? This lecture contains:- 1.Definition and understanding of solution 2.Diffe... In the Brønsted-Lowry definition of acids and bases, a conjugate acid-base pair consists of two substances that differ only by the presence of a proton (H⁺)....
