I am asking here because I only have a highschool level of Biochemistry knowledge. I do understand that Caffeine blocks adenosine receptors in the brain, but I don't understand how that has a correlation to "long term effects" like positive effects or negative effects in moderate use.

Even in moderation consumed daily, it means that the body is always more stimulated than it should be, and so blood pressure and the entire sympathetic system is alert even somewhat. I don't understand how having that makes you less likely to have a heart attack in the long term, for example. Even if a healthy body doesn't mind constricted blood vessels most of the day, I don't see how that can have a positive effect.

Leaving the body itself aside, what about the brain? How does blocking adenosine receptors constantly "lower the risk of dementia?". All the papers I'm finding online are just finding correlations between the two but aren't actually explaining it from a biochemical standpoint. What is it about having blocked receptors that changes the brain to such an extent that it's less likely to be damaged?

this bothers me a lot and I can't seem to find the answer. Is it because they worked only on the bacteria present in animals such as Mycoplasma bovis?

I have always wondered why parenteral solutions of whatever drug are always manufactured as colorless agents. Is this merely due to psychological reasons since people associate purity with transparent solutions, or is it because there simply is no dye, natural or synthetic, that is harmless to the organism when injected?

I'm asking because I thought it would be a pretty simple and cost-effective way to distinguish ones product from the same product that another pharmaceutical company is selling. To give you an example: the company I worked for specializes only in the manufacture of opioid medications (and patent licensing, but that's only a small portion of the revenue), and while the peroral dosage forms all come in different colors, the injectable solutions all look colorless and are virtually indistinguishable from the competitor's products. Is that because there is no dye that is non-toxic for injection?

Is there a name of a terminology for when you give someone a specific GABA drug and and a few hours later dopamine is released? For example GHB and phenibut will do this.

Thank you in advance.

I am currently trying to evaluate a paper regarding novel drug release but while reading it i saw quite the variance in the loaded amount and release between batches using a chemioterapic.

Is there a database where given the name of a certain drug you can easily get a LD50?

Hello I’m currently looking to switch from my biology bachelor program to a pharmacology and toxicology bachelor program that is online. During that time I have a Lab aide job set up to gain experience and years while also going to school. I was wondering what type of job opportunities I would be looking at after just achieving the bachelors in pharmacology and toxicology. As well as afterwards getting it is it necessary or should I go to a program afterward for furthering either pharmacology or toxicology. Or is it possible to even obtain some certifications and go further as well afterwards. I just want to know how my future would be like if anyone has done similar, and if I have to go to more school afterwards.

Does anyone happen to have information about reimbursement of thalidomide/contegran/distaval from the 1950-1960s before it was retracted from the market? I'm really struggling to find any information on it for my paper.

I did TLC on starch but the RF value that i got was 0. I can't find a standard RF value of starch in the Handbook of Pharmaceutical excipients.

Is that normal or am I doing something wrong here?

Any references that you can recommend to me?

thank you!

Hi, I’m looking to enter the pharmaceutical industry in the future and I have some questions relating to choice of university and job prospects, hope that the community can help provide some insight into my doubts 🥺

I would most greatly appreciate you taking the time to read through some of my concerns :)

I’m currently a Singaporean citizen looking to enter university. I have 3 options:

1. NUS with full scholarship studying Pharm Sci, graduating with Bachelor with Honours
2. Imperial College with no scholarship studying Chem w Medicinal Chem, graduating with MSci with honours
3. UCL with no scholarship studying Pharmacology, graduating with Bsc/MSci

Motivations for overseas (please do evaluate how realistic they are):

1. Gain access to the UK market, and by extension, easier to enter EU market
2. Uni has a better reputation (but it’s also not by a lot, unsure how industry treats a NUS vs Imperial/UCL grad)
3. Learn how to be independent

Drawbacks:

1. Insanely ex, tried applying for scholarships but there isn’t much available anyway and because Singapore doesn’t count as a developing country so a lot of financial aid isn’t applicable

Apart from that, my main worries are about job prospects in UK. Could anyone in industry shed some light on how receptive pharma companies / branches in UK are to sponsoring a tier 2 visa for an international graduate? Although I’m aware of the skilled workers visa that allows for 2yrs of work, I heard there’s a minimum of 38k salary a year, I’m not sure if companies are willing to provide that sort of salary to a fresh grad.

Is the Pharma industry good in the UK compared to SG? And in general is there a substantial difference in salary and treatment in graduating from NUS vs Imperial/UK? If so, is it worth the 350k SGD I have to pay for a UK uni? Because this sum is by no means small for my family and I would not want to burden my family if I finish my uni in UK and in the end come back to SG if I can’t land a job in the UK.

Are there higher barriers to entry to the UK US market having graduated and mainly worked in SG compared to graduating from a UK Uni?

I also have some plans for future development, wanting to work in management in the future. What are some advice you would give to head in this direction?

And last but not least, between Imperial & UCL, which would be a better option to enter the Pharma industry, I have heard Imperial with a broader course allows for more flexibility but UCL goes more in depth into Pharmacology. Is it also worth it to take a gap year to do a year long internship since that would extend my studies by a year.

Sorry if I have bombarded you with so many questions but these are some burning qns that after scrolling through the Internet, I haven’t gotten a satisfactory answer to. Thanks for taking the time to read through and greatly appreciate your answers!

What purpose does this specific dosage serve?

Why does nothing happen to cyclooxygenase, although glucocorticosteroids inhibit phospholipase A2, which is preceded by COG1-2?

Hi Everyone!!

So im really interested in studying biochemistry(currently a junior in HS) and pharmacheucetials, I would like to go into lab research. Im a little confused on the programs I need to take and the length of this process. If I want to go into pharmaceutical research, I would first have to do an undergrad of a related field like bio or chem and then go to grad/pharmacy school which would take like 8 years. Am I correct?

Are there any programs that are accelerated or fast tracking? Or any suggestions or programs or opportunities I should look into? ill be going to uni in Canada btw :) (dream school is definitely queen's uni)
Thank you so much for your time and help!!

There are well-known inhibitors of 5-alpha reductase such as finasteride and dutasteride.

However I’m wondering about the opposite case: is 5-alpha reductase available for administration, for example if someone has a deficiency? I haven’t found any resources on this.

I’m not saying this is a good idea, necessarily, but am just looking for availability of 5-AR. I’m not asking for specific sources either.

Hello, if this isn’t the best place to post, my apologies.

I’ve been out of college for 2 years now and working in a field that isn’t quite where my heart lies. I graduated with a Bachelor’s in Psychology, but the last year of my degree was entirely related to pharmacology and neuroscience. I was captivated, and aced all of those classes, and found a new motivation where I was previously graduating just to be done (I was a super duper duper senior). My only question I suppose is, is the title a good fit? I’ve been recently looking into Graduate schools because I want to get into the field that interests me. My biggest interest is research in neuroscience and neuropsychology. Especially in the aspect of drug testing and drug trials, and research into application of drugs for treating neurological disorders.

The reason I ask is because as Ive been out of academia for awhile, the sense of direction and guidance to it has been difficult to assess. I know what I want to do, but not how to get there and the best steps.

I'll keep this brief...

I am coming to the end of my first year studying medical pharmacology at university, I am honestly slightly overwhelmed with the sheer amount of biology that I have had to/ will have to learn. This semester I have a class in organic chemistry, and upon sitting down to do my first major assignment, I was actually enthusiastic about completing it.

Generally speaking I just hate rote learning or whatever you want to call it, I like to apply knowledge - and when I have to learn it I want to know why its important for me to learn and I want to understand so it becomes slightly easier for me to recall the next time around.

My degree seems to be full of biology, and very little to no chemistry. In the first year. Does it get better as I progress further into the field or have I gone and chosen the wrong degree?

(I don't mind biology it's just the sheer amount of it...!)

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I can't wrap my head around why patients who take pyridostigmine, such as in Myasthenia Gravis or Alzheimer's, will 1.) have a prolonged effect of succinylcholine and 2.) a relative resistance to non-depolarizing neuromuscular blocking agents.

Pyridostigmine --> inhibits breakdown of acetylcholinesterase = more acetylcholine available in NMJ.

Succinylcholine is metabolized by pseudocholinesterase. Does pyridostigmine also inhibit pseudocholinesterase? Is that how it creates a prolonged effect of succinylcholine?

I don't understand how it creates a resistance to non-depolarizers.

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I am new to Reddit so please excuse me if I should be directing this question to another community. Thank you.

Here is the published abstract:

Abstract

A retrospective (N = 140) and a prospective (N = 102) observational Israeli study by Bar-Sela and colleagues about cannabis potentially adversely impacting the response to immunotherapy have together been cited 202 times, including by clinical practice guidelines. There have also been concerns on PubPeer outlining irregularities and unverifiable information in their statistics and numerous errors in calculating percentages. This reanalysis attempted to verify the data analysis while including non-parametric statistics. The corrected prospective report contained 22 p-values, but only one (4.5%) could be verified despite the authors being transparent about the N and statistics employed. Cannabis users were significantly (p < 0.0025) younger than non-users, but this was not reported in the retrospective report. There were also errors in percentage calculations (e.g., 13/34 reported as 22.0% instead of 38.2%). Overall, these observational investigations, and especially the prospective, appear to contain gross inaccuracies which could impact the statistical decisions (i.e., significant findings reported as non-significant or vice-versa). Although it is mechanistically plausible that cannabis could have immunosuppressive effects which inhibit the response to immunotherapy, these two reports should be viewed cautiously. Larger prospective studies of this purported drug interaction that account for potential confounds (e.g., greater nicotine smoking among cannabis users) may be warranted.

Overall, the two prior studies, and especially the prospective one, were riddled with errors.

Anyone surprised?

Here is the free full-text:

https://www.mdpi.com/2072-6694/16/7/1245

Hi, I am studying for an exam, and found two conflicting answers for this question. Which is the correct answer,

A. Tamsulosin B. Bethanecol C. Methacoline D. Terazosin

One book says Option A is right. The other Option B. I don't trust me reasoning enough and am too anxiety riddled to trust anything I think. I just need a consensus on this. Thank you.

Where can I typically find the dose-response relationship for a newly approved drug from the FDA? I know pharma companies will usually collect data on this during their clinical trials and submit this information to the regulatory body to get approval, but does the FDA publish this data? SPC doesn't seem to have this piece of information. 

There is a lot of data, mostly in animals, some in humans, of negative effects of antibiotics on male fertility. Often, these effects are found to be reversible, given sufficient time, but the data seems to be quite limited and studies often do not check whether the effect, once found, is reversed. From the literature I've read, the consensus seems to be that there's inadequate data to conclude whether some antibiotics may have a permanent effect.

Is anyone aware of studies that have found a permanent effect, whether in humans or animals?

Also, any comments and thoughts you may have on this matter and how likely it is that there is a permanent effect, I would be curious to hear.

There are two studies I've found which found an irreversible effect.

#1 A permanent effect in rats, but the drugs were administered in pre-pubescent rats, so it's possible there was damage to the developing reproductive system and that if the same drug were administered to sexually mature animals, the effect would not have been permanent, but this is speculative.

#2 A permanent effect in rats given rifabutin.

Hello there!

I want to get more into pharmacology. I'm currently in the process of applying for pharmacy schools, because some of the info I found online is that a PharmD is a good step. Is transitioning from Pharmacy to Pharmacology a reasonable/possible thing to do or should I just drop the idea and follow another pathway?

I didn't do any research outside of labs in college due to some personal stuff, so I don't think I could get into a graduate school other than Pharmacy school but I do find the process of drug development/production interesting and want to explore it further.

Maybe this isn't the best place to post this, but any advice and thoughts would be welcome! Thank you for reading this!

Hi, I’m a pharmacy student and as a part of our medicinal chemistry course we have to investigate why the carboxylic acid bonded to the pyrrolidine has a lower pKa than “usual”. Enalaprilat has two carboxylic acids, the one “closer“ to the bencene that has a pKa of 2,3 (which is lower than the 4 expected for a carboxylic acid, but thats because the conjugated base of the carboxylic acid forms a cycle with the hydrogene from the nitrogen next to it) but, the other carboxylic acid has a pKa of 3,4 and I don’t really know what makes it to be lower than 4, why is it more acid than usual?? theres no more resonance structures, and as far as I know nothing is giving it electronic density. If someone could help me understand would be awesome, thanks (also if the post should not be here, I’ll delete it)

Hi Everyone!

I'm a junior in high school, and I really want to pursue biochemistry and go into pharmaceuticals. However, I'm a little confused about the path I should take. Some people are saying I need to do a Ph.D. The school I want to go to said I need to take health sci as an undergrad and then apply for biochem, which confused me even more. Originally I kinda thought I could go into pharmaceuticals with a biochemistry degree.

What education is required to become a pharmaceutical research scientist? Thank you!!

The image bellow was taken out of Goodman. It explains the mechanism of action of trimetoprime and sulfonamides in inhibit "folate metabolism". Why is it called so? I can't get it, because in the image we see the byproducts not of folate, which is PABA + pteridin + glutamic acid, but those of PABA + pteridin, which makes dihydropteroic acid.

Why are they said to inhibit folate and not dihydropteroic acid?

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https://preview.redd.it/l9jvfbfsbxoc1.png?width=679&format=png&auto=webp&s=51fc91ba23d6863b521b4480361fb94eab7040c5

I've been looking into Talicia, a single capsule formulation of rifabutin, amoxicillin and omeprazole which was recently marketed for H. pylori treatment and I noticed that in the documentation for their phase III study, under inclusion criteria, they state:

Males must be surgically sterilized or are prepared to and agree to practice double method (barrier plus spermicide) birth control from screening through to 30 days post-EOT

This got me wondering what required this condition and it turns out that much of the documentation for rifabutin states the following:

Fertility was impaired in male rats given 160 mg/kg (32 times the recommended human daily dose).

You see this statement repeated over and over again in various rifabutin-related documents. Now, I'm not 100% sure what the source is for that statement, but the only study I've been able to find is this one and it says:

An effect of rifabutin on male gonads was observed in some rats at the dose of 200 mg/kg given by gavage for 13 weeks, and at 80 mglkg in the 52-week study. This effect was a bilateral, focal or diffuse reduction of spermatogenesis, which showed little tendency to regress. More- over, signs of testicular atrophy were seen in the carcino- genicity study in the same species in the high dose group of 60 mg/kg. Functionally this change was reflected by a reduction of implantations in the fertility study with males treated at 160 mg/kg.

I know these are larger doses than given to humans, nevertheless, a little worrying. As best as I can tell, male fertility has never been studied following administration of rifabutin in humans and Talicia simply states flatly:

Based on findings in rodents, drug may impair fertility in males of reproductive potential

Isn't this something that should have been studied, considering the severity of the potential effect and its apparent irreversability(!)? Are there human studies that maybe I've just missed?

I've been trying to find the info for the solubility of amoxicillin trihydrate (from a dispersable tablet) and while I found a source that summarizes the results of a number of studies (table 1), none of them were performed at the natural pH of tap water and at room temperature (around 20 C).

Does anyone know where I might find such info?

Hello everyone, I wanted to know if it is true that methyl esters are pro drugs, which once ingested, are hydrolyzed and transformed into the reference molecule. this hydrolysis can occur both in a basic environment (intestine, bile, blood) and in an acidic environment (stomach) and this transformation occurs thanks to the esterase enzymes which are ubiquitously present in the body, so much so that esterification can also occur in the case of topical, intramuscular, rectal administration etc. the esterase enzyme manages to replace the -CH3 group with the -OH group.

1. Is this a reaction that occurs for all methyl esters or are there exceptions?
2. methyl esters can't have any pharmacological activity right?
3. for example methylcobalamin will be transformed into cyanocobalamin or am I wrong?
4. Are all the molecules sold in methylated form which are declared more absorbable than the basic versions just commercial speculation without scientific basis? Thanks for help

if a drug was selective for Receptor 1 with log[Drug] of -9, and Receptor 2 for -8, how many fold selective is receptor 2 for the drug than receptor 1?

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Hi everyone, I am currently in a pharmacology course while I wait to get into Nursing school. I have an upcoming midterm and am wondering if anyone has any good study tips, sources, or mnemonics to share. We are covering so many drugs its hard not to confuse which are for what and to remember the brand and generic name and MOA. Looking for any suggestions!

Hello everyone,

I was talking to a friend about aspirin and I discovered that there is a liquid version, called lysine acetylsalicylate, which is a soluble salt of aspirin that is used intravenously. Apparently it is a very important drug, but not many places make it. Bayer did, but they are selling their production facility to a third party (or something to that effect). So my question is, why does no one else make it? We are talking about aspirin, which is not new and I think the lysine form as well, so patents should not be an issue. So my questions are:

1. why are there only a handful of suppliers? If any apart from Bayer?

2. Is it a particularly difficult formulation to make? If so, why?

Thanks in advance to anyone who answers!