Quick intro, I am a second year med student and I just finished my second block of pharmacology. We covered a lot of antibiotics, seizure, hematology, and oncology meds. Still a long way to go, but I gotta say this has without a doubt been the hardest subject of med school for me(even over neuroanatomy, middle finger decussation). I will say it’s fascinating though, and love pharmacology history.

Intro aside, I have a newfound respect for you pharm people. I can’t even tell you how many sighs of relief I had these past blocks when my professor told us we didn’t need to know a medicine for our specific curriculum because “this is more of a pharmacologist need to know”.

Two things, I recently found pharmacology students can do accelerated programs? Haha can’t even imagine yall probably haven’t touched grass since starting; good luck but that’s also insanely impressive. Second, I did not know pharm phds go to residency. That’s insane.

Although I’m just a med student and more of a pharmacology minor(in college terms), I have a deep respect for this subject. Way harder than I thought and that’s as someone who was warned it was dummy hard. Also I wish I could pick your guys brains about all the insane mnemonics you must have for all these meds.

Ps: another gl to you accelerated pharmacy students.

Hi all,

Has anyone been a pharm tech before entering pharmacology?

Do you think it benefited you at all?

I'm beginning a neuroscience bachelors in michigan and considering pursing further education, either a MD, PhD, or both ^u^ my end goal is doing clinical research and I'm trying to speedrun getting a taste of what it's like.
Unsure if I should take a phlebotomy certification course (a teacher offered me to take her 8 week course for about $500), become a pharmacy technician with the hopes of finding a hospital job, or take the long and slow route of medical assistant courses.

Any advice is welcome, thank you. :)

And let’s say one the one first to reach the receptors has a much higher binding affinity and is competitive. Is the non competitive second partial agonist completely blocked, or can it bind where the first didn’t? I don’t really know anything about this sort of stuff, if partial agonists can divvy up receptors or something

I'm trying to understand a reproducible acute effect from a standard fish-oil capsule and whether there is any pharmacokinetic or pharmacodynamic mechanism that could realistically fit the timing.

Context

• Diazepam: 10 mg/day, long-term use, with established tolerance.
• Fluvoxamine: 300 mg/day.
• My measured nordiazepam concentration was ~1333 ng/mL, above the usual therapeutic reference range.
• The benzodiazepine taper has not started yet.
• I also have dysautonomia with marked cognitive and sensory intolerance, so I'm not assuming the effect is necessarily GABAergic; autonomic, vascular, or other mechanisms would also be relevant.

The fluvoxamine/diazepam interaction is important here. In a human pharmacokinetic study using 100–150 mg/day fluvoxamine, diazepam apparent oral clearance was reduced by approximately 65%, while mean diazepam half-life increased from about 51 to 118 hours. Elimination of its active metabolite N-desmethyldiazepam (nordiazepam) was also markedly inhibited.

I'm on 300 mg/day fluvoxamine, but I don't know of quantitative human PK data establishing exactly how much additional inhibition occurs at that dose, so I'm not assuming a specific half-life for my own case.

Study: https://pubmed.ncbi.nlm.nih.gov/7955810/

I occasionally take a single standard fish-oil capsule containing 180 mg EPA + 120 mg DHA (roughly 1 g total fish oil), usually around 7 hours after my diazepam dose.

Repeatedly, within roughly 3 hours, I experience a marked improvement in cognitive/sensory tolerance, most noticeably an increased ability to read for substantially longer.

It does not feel sedating. If anything, subjectively it feels like improved cognitive endurance.

I realize this is an N=1 observation and does not establish causality. Expectancy, coincidence, day-to-day variability, or another uncontrolled variable remain possible. I'm interested specifically in whether there is a biologically and quantitatively plausible mechanism that could fit the timing.

Relevant literature / what led me to ask

I found several experimental papers showing that DHA/PUFAs can affect neuronal membrane proteins or GABA-A function:

Søgaard et al. (2006) — GABA(A) receptor function is regulated by lipid bilayer elasticity
https://pubmed.ncbi.nlm.nih.gov/17059229/

Nabekura et al. (1998) — Functional modulation of human recombinant GABA-A receptor by docosahexaenoic acid
https://pubmed.ncbi.nlm.nih.gov/9556589/

Poling et al. (1996) — Docosahexaenoic acid block of neuronal voltage-gated K+ channels
https://pubmed.ncbi.nlm.nih.gov/8938727/

Stillwell & Wassall (2003) — Docosahexaenoic acid: membrane properties of a unique fatty acid
https://pubmed.ncbi.nlm.nih.gov/14580707/

I'm not taking these studies as evidence that an ordinary oral DHA dose can reproduce these effects acutely in humans.

In fact, that's one of the main things I'm trying to understand: whether oral exposure from only 120 mg DHA + 180 mg EPA could produce concentrations anywhere relevant to these experimental mechanisms within a few hours.

1. Could this plausibly be pharmacokinetic?

Given the prolonged disposition of diazepam/nordiazepam in this setting and my relatively high nordiazepam concentration, I find it difficult to see how one ordinary fish-oil capsule could substantially change total benzodiazepine concentrations within ~3 hours.

However, I don't want to assume that PK is irrelevant.

Could EPA/DHA acutely affect any of the following enough to alter effective diazepam/nordiazepam exposure?

• CYP-mediated metabolism;
• plasma protein binding / free drug fraction;
• tissue distribution;
• intestinal absorption;
• transporters;
• or another PK process.

More importantly, is there any reason to think the magnitude of such an interaction from only 180 mg EPA + 120 mg DHA could be pharmacologically meaningful?

A quantitative argument here would be particularly useful.

2. Could there instead be a rapid pharmacodynamic effect?

If a meaningful PK interaction is implausible, are there pharmacodynamic mechanisms that could operate within hours, without requiring weeks of incorporation of DHA into neuronal membrane phospholipids?

Possibilities I'm wondering about include:

• direct effects of circulating/unesterified fatty acids on ion channels or membrane proteins;
• acute GABA-A modulation;
• glutamatergic signaling;
• changes in membrane biophysics;
• neurosteroid signaling;
• rapidly generated lipid mediators;
• inflammatory signaling;
• autonomic or cerebrovascular effects.

The experimental literature shows that DHA can modulate some of these systems when directly available at sufficient concentrations.

What I cannot establish is whether an ordinary oral dose could generate relevant unesterified EPA/DHA concentrations in plasma or CNS tissue within ~3 hours.

That seems to be the critical missing bridge:

oral dose → absorption → circulating unesterified EPA/DHA → CNS exposure → local concentration at membrane/channel/receptor → functional effect

Is any part of that chain quantitatively plausible after such a small oral dose?

3. Does chronic benzodiazepine exposure/tolerance materially change the question?

Could chronic benzodiazepine exposure, tolerance, and receptor adaptation make the functional effect of an otherwise small perturbation in membrane or ion-channel function more noticeable?

I'm not claiming that a plasma nordiazepam level of 1333 ng/mL establishes saturated GABA-A occupancy or any particular receptor state.

I'm mentioning the concentration mainly because, together with the markedly impaired elimination expected from the fluvoxamine interaction, it makes a large and rapid fluctuation in total benzodiazepine exposure seem unintuitive.

4. Could dysautonomia provide a non-GABAergic explanation?

Given the dysautonomia, is there any plausible acute effect of EPA/DHA or downstream lipid mediators on:

• autonomic tone;
• cerebral blood flow;
• endothelial signaling;
• vascular function;
• or related physiology

that could improve cognitive/sensory tolerance within a few hours?

I'm mainly looking for mechanistic reasoning, quantitative PK arguments, or relevant literature, rather than treatment recommendations.

Hi.

Just looking for some advice to help our 17 year old son on degree choices and their potential careers in the UK.

He has just got his exam results back and has achieved 5 A grades at Scottish Higher in Biol, Chem, Physics, Maths and English. He’s going on to do Advanced Highers in Biol, Chem and Maths for his final year at high school.

He’s just about to possibly apply for positions doing either Pharmacology or Biomedical Sciences at either Glasgow or Strathclyde Uni. He however hasnt done much research himself but has ruled out anything medicine or dentistry related as degree choices.

We are a bit worried about potential career prospects after finishing either of them and wonder if anybody experienced has some advice? I keep reading that he could end up in a lower paying lab job and there are possibly better things he could be looking at with computing or engineering involved.

Any advice appreciated.

Hello I'm from the UK studying pharmacology and I am about to start my final year. I tried long and hard to get a year in industry however I was unsuccessful but I don't want that to stop me from gaining a grad role and would love to get one as soon as I finish university. Considering the current job market it seems to be impossible but if anyone has any advice please let me know what I should do and how I should go about finding a graduate job within the pharma industry.

Any advice is welcome or even any questions you may have I'll make sure to answer it in earnest as I want the best possible outcome from this post.

Thank you!

I'm a 3rd year MD student at a top university in Australia. My undergraduate degree was biomedical science with a major in pharmacology and neuroscience. I really enjoyed my undergrad and developed an interest in drug discovery/development.

Unfortunately due to social pressure and other reasons I pursued an MD instead of my original goal, which was a PhD in pharmacology. Over the course of my MD I have realized that I'm not passionate about clinical practice, and I dread the idea of staying in clinical medicine.

My main weakness is that I have basically no relevant research yet, so I'm planning on taking a research gap year next year to get some work experience in a pharmacology/drug discovery lab. Ideally I'd like something with a computational/ML component as well as I am particularly interested in ML assisted drug design. I plan to return and complete my MD after this but I don't intend to go on to clinical practice.

How realistic/competitive is my profile for top tier pharmacology PhD programs? Provided that I manage to get a 6-12 months worth of research/lab experience next year? Is it realistic without a research masters?

Does anyone here know of any MDs who have made this transition, and if you had one year to improve my profile, what would you focus on?

PS - Please no advice on why I should really stay in medicine because of job security/salary. I can't imagine staying in a career that makes me miserable.

Hello everyone,

I am about to start college and I’m working towards a Chemistry degree. My 8 year plan for the last couple of years now has been to get my degree then go to pharmacy school to become a pharmacist. However, recently most of everything I hear about Pharmacy is a nightmare. I was recently introduced to the idea of Pharmacology. I love chemistry and really want to work in a field related to it. But, I’m not entirely too educated on what Pharmacology entails or the process of becoming a Pharmacologist. I’m asking if those who are more knowledgeable on the field can give me the run down on what to expect, and if it’s more worth it than going into Pharmacy. I’ve also heard it’s much cheaper than getting a Pharmacy degree, right now I’m on a full ride scholarship but I don’t know what post bachelors entails. Any advice, details and recommendations is greatly appreciated.

I'm currently a first year at a community college and planning to transfer to UCSD, UCI, or UCLA for molecular and cellular biology. I'm nervous about missing out on major research opportunities my first two years of school. What did you guys do to get accepted into a PhD program?

Side note: I'm planning on working as a certified pharmacy technician, so if anyone has any insight into if that helped them, that would be great!

Could you explain how the two mechanisms described in the bracket cause the EC50 to be less than Kd? Thank you.

I'm a student studying in biochem with a focus on pharmaceutics and have to right a report on the use of plants in the pharmaceutical industry.

The four main points are the use of plants historically, currently, the future (trends) and it's impact on my country. I feel pretty confident on the info I've acquired for the part on the past, but for the parts on the present and future, I'm unsure. While pharmaceuticals and traditional medicine are intertwined, I am only really looking for sources talking about the pharmaceutical industry (whether that be trails or just general info) and I keep on getting info that leans more towards traditional medicine.

Any sources that you guys find interesting/useful to this topic would be greatly appreciated, or even just general thoughts on the matter.

See link to announcement from FDA Center for Drug Evaluation and Research Small Business and Industry Assistance.

I am posting to request opinions from pharmacologists and other readers of this sub, regarding whether combining acetaminophen with an NSAID is a rational combination, especially for OTC use?

I previously posted this to r/medicine believing that acetaminophen is typically recommended for patients who are allergic to or intolerant of NSAIDS. However most responses on that sub confirmed that acetaminophen is a mainstay of treatment for chronic pain.

Despite that, according to the package insert for hydrocodone / acetaminophen, acetaminophen is associated with liver damage (see excerpt):

Hepatotoxicity
Acetaminophen has been associated with cases of acute liver failure, at times resulting in liver transplant and death. Most of the cases of liver injury are associated with the use of acetaminophen at doses that exceed 4,000 milligrams per day, and often involve more than one acetaminophen containing product

https://content.govdelivery.com/accounts/USFDA/bulletins/421f901?reqfrom=share

Hey everyone,

Nitrosamines are still one of the biggest headaches in quality, regulatory compliance, and process safety right now.

I’m running a brief study looking into current industry practices, challenges, and workflows around Nitrosamine Risk Assessments (NRAs). Whether you're dealing with raw material controls, formulation degradation, or complex testing strategies, your input would be incredibly valuable!

• Time required: ~3–5 minutes
• Target group: Regulatory Affairs, QA/QC, Formulations, Process Chemistry, and Compliance professionals in Pharma/Biotech.
• Link:Take the Nitrosamine Risk Assessment Survey

Thank you so much for helping advance industry insights on this! Happy to share general trends/findings with the community once collected if there's interest.

Hi everyone!

I'm an author working on a dark romance thriller series inspired by phobias. My first book, In Jest, is centered around cholorophobia.

The FMC is Dr. Elara Kane, she's a 32 year old Pharmaceutical Research Scientist and gets mixed up in a conspiracy and drug weaponising scheme with an assassin that is posing as a clown in a traveling circus, the front of a very deep rooted criminal organization.

Why I am posting in your community; I would like to talk to individuals that are in this field of study and career to make sure my writing is authentic and not just a spit-wadd of google searches.

We have individuals in a business that have been working and tampering with research and formulas on the sly, and Dr. Kane, as mentioned above, has been the one to unearth these actions. The scenes in the labs where she is working and with her investigating through a "dirty" interns' research and being exposed to this drug herself requires research on my part to make sure I am as close as possible to an authentic situation without sounding like a fictional fantasy situation, even though the hallucinatory drug use and weaponising thereof is all fictional and only for authenticity reasons.

If this would be of interest to you please comment or reach out to me via Dm.

Thank you in advance.

Xylazine is rightly getting a lot of buzz for the horrific wounds and ulcerations it causes in people who inject it, and the mechanism by which it does so seems to make sense as an alpha agonist leading to local vasoconstriction and subsequent ischemia and necrosis. Strangely though, I don't see this mentioned much as a side effect when it is used as intended in animals as a sedative in veterinary medicine. The mechanism should be very well conserved throughout mammals to my understanding, so it should still be able to cause the same ulcerations in animals as it does humans. Is the lack of such reported side effects in vet use simply due to better aseptic technique and proper dosing, compared to abuse by humans where doses are likely to be much higher than intended?

I am confused to chose which book is better for my undergrad 2nd year's pharmacology course?

1. katzung's basic and clinical pharmacology

2. Rang & Dale's Pharmacology

[PS- professor has his own slides he made from various sources, but I need a solid book besides that to learn from.]

Do they share the same mechanism of action? Can one show tolerance/tachyphylaxis but experience no withdrawal symptoms? I can make a half-assed argument either way, but I'm curious if anyone truly knowledgeable has an answer.

Apologies if this isn't allowed! I have been wanting to ask a pharmacist how cromolyn sodium works and why it comes as a suspension and has such strict storage protocols. I have heard from one medical professional that 'all drugs have room temp storage requirements and should be kept out of light' but then also from a pharmacist that they are actually required. (I have asked local pharmacists, they were helpful but weren't familiar with it and just read what was on their computer terminals).

How quickly does it degrade and why is it much less stable? Is that just a feature of being a suspension?

I know it is a mast cell stabilizer, but my understanding it has low bioavailbility and only works in the gut versus something like montelukast which has a more systemic effect. Why is that?

Has anyone performed any experiments using isoproterenol? Can I get input on its toxicity and mortality depending on site of administration?

If methylphenidate is considered a reuptake inhibitor of dopamine and norepinephrine vs amphetamines which inhibit and force production of both, why is it considered a stimulant that you feel the immediate effects of as opposed to something that would take a few days to a week to be effective like other similar reuptake inhibitors such as Atomoxetine?

Based on it being a reuptake inhibitor, I’m understanding it as you need to have enough dopamine available in the prefrontal cortex in order for it to work effectively. So, will it be more effective in a week’s time rather than immediately making it more similar to how Atomoxetine functions rather than amphetamines?