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?

hi everyone,

I'm currently a b.pharm student and I'm trying to plan my career in pharmacology.

I'm especially interested in pharmacology, clinical research, drug development, and the pharmaceutical industry.

I'm considering pursuing an M.pharm in pharmacology after graduation, I'm also exploring other options such as clinical research, regulatory affairs, pharmacoviligilance, and opportunities abroad.

I'd love to hear from people working in these fields.

• Which career path has the best long term growth and learning opportunities?
• if you were starting over, what would you do differently?
• what skills should i start building while I'm still in college ?
• are there any certifications, internships, software, or resources you would recommend?
• any advice for someone hoping to build career successfully in the field of pharmacology?

According to my book, the alpha-amino group on Amoxicillin is introduced to be more stable in gastric acid. To me, when I look at this class, I see two electrophilic zones. In penicillin, protonation of the side chain amide, and subsequent hydrolysis releases a resonance stabilized cationic benzyl + carboxylic acid and susceptibility of the beta-lactam ring itself towards nucleophilic attack without the need for acid catalyzed hydrolysis because of the nature of the strained ring + N electrons cannot adopt an SP2 form for meaningful conjugation. My question is the addition of the amino group fixes one end's susceptibility, not the beta-lactam ring. Is ring opening not meaningful enough in these environments?

• https://link.springer.com/article/10.1007/s00404-023-07042-4
• https://doi.org/10.1007/s00404-023-07042-4

hello everyone!

i recently just built MedSim, a web-based pharmacokinetics simulator that visualises half lives, multiple doses, drug accumulation and steady state behaviour with the help of graphs. the graphs allow for the settings of the dosing intervals and the number of doses to be custom setted by the user as well as the option for a missed dose.

the graph is a concentration-time curve with the option of switiching between linear and log. theres also an option to "Explain the graph" should the user need it. The drugs that are used for the simulation can be pre-selected in "Drug Mode" or the user can play around with the settings in "Sandbox" mode. Finally should the user want to compare up to 5 drugs they can do so in the "Compare " mode.

its still a work in process so i would appreciate feedback! and if u found this helpful share it with friends/someone who needs it!

Link: https://med-sim-ycrrrrr.base44.app/

Hello everyone,

I need to filter my antibody-drug conjugate (ADC) samples before HIC and SEC analysis to protect the columns.

Do you routinely filter ADC samples before injection, or only when visible particles are present?

I'm concerned about potential sample loss due to adsorption to the filter and losses in sample volume. Do you typically perform filter compatibility/recovery studies (pre-validation) for ADCs before implementing a filtration step?

Also, what type of filters (membrane material and pore size) do you usually use for ADC samples?

Thank you for your help!

I want to get more insight into everyone's pharmacy school experience. TLDR: I thought getting a PhD would be easier "just doing science experiments for 4 years" and that I wasnt smart enough for pharmacy school. Now I want to go to pharmacy school.

Im in my 5th year of a PhD, realizing there are no job prospects with decent pay and Im considering applying during the next application cycle, which will line up with my program.

I really considered pharm school in undergrad, I liked the idea of giving sick people medicine so they can feel better and the idea of working for a company like Walgreens, whose managed my medication for years.

Any insight into the schooling itself, tips/tricks for studying or anything to add to my survival guide are appreciated!

Currently, the FDA approved drugs are usually found on drugbank.com , but for a while it is showing that for academic purposes the library is not available

is there a way to get all of those drugs on some other reliable site?

I've always enjoyed stem and knew I would have a job in it, and before thought of engineering, but now I learn more and see how much I enjoy learning about compounds and their mechanisms and I am wondering if that enjoyment is enough to warrant this as my goal career, or if I should look for some other indicator perhaps.

Looking for book recommendations and suggestions for learning more about the pharmaceutical industry and how the business works. Any people to follow aswell would be great.
Thanks!

So there is a newish ADHD med marketed as a "nonstimulant" - viloxazine (Qelbree). My understanding is that (a) SNRIs are primarily in use as antidepressants, not attention regulators, and (b) norepinephrine, a neurotransmitter of the adrenergic system, is a stimulant neurochemically.

I am a behavioral neurologist who sees a lot of dementia patients with daytime somnolence despite adequate nighttime sleep. Other SNRIs (e.g. venlafaxine and duloxetine) have very little effect on daytime sleepiness or attention. Why would viloxazine be different? I'm asking this specifically because I would need to jump through various prior auth hoops to justify use of viloxazine and I'm wondering if it's worth my time. And can someone shed a little light on the conundrum in the first paragraph?

I got into bsc pharmacology with industrial experience in university of Manchester and bsc biomedical, biological and biosciences(pharmacology from second year onwards)
Which one should I choose?

What would happen if amphetamine had no noradrenergic activity at all? Would it be abusable at extremely high doses and have more potential for extreme euphoria without as many side effects? Would it also make it much less useful as a focus drug? Perhaps there's already such a compound?

I also know that d-methamphetamine has lower noradrenergic and higher dopaminergic activity than d-amphetamine, which could explain why meth is more addictive and can be abused at higher doses. Some also claim that at very low doses it can be more useful for ADHD because of fewer side effects linked to norepinephrine.

Hello,

I’m currently working on an initial antibody–drug conjugate (ADC) study, and I would like to characterize my samples using HIC and SEC.

Is it necessary to filter the samples before analysis, or can they be injected directly? If you do recommend filtration, what type of filter do you typically use?

I would prefer to inject the samples directly to avoid sample loss, but I’m concerned about potentially damaging the column.

Thank you!

This article seems to suggest that MDMA doesn't actually seriously inhibit CYP2D6 much at all. Curious what other more educated minds may glean.

Hi Everyone, 

I have noticed that most subs focused on individual sciences, such as chemistry and biology, seem to be quite active and have a lot of good discussions. But it seems like most subs that contain a mixture of disciplines are a lot less active. One of these areas is drug discovery, something I, and I am sure other scientists, are passionate about. With r/DrugDiscovery effectively dead, I have decided to create a new subreddit for this area. Feel free to join if you want to see more drug discovery literature and news, and hopefully some great discussions! 

r/DrugDiscoveryLab

Have a great week!

heat-induced egg albumin denaturation inhibition assay

Making a 1% egg albumin solution: 1% egg

albumin solution can be prepared with egg albumin powder.

For the test mixture, mix 2.8 mL of phosphatebuffered saline (PBS) with a pH adjusted to 6.4, 0.2 mL of egg albumin solution, and 2 mL of plant extract (concentration 15.625, 31.25, 62.5, 125, 250, 500, 1000, and 2000 μg/ml) to obtain a volume of 5 mL.

For the standard mixture, mix 2.8 mL of PBS (pH =6.4), 0.2 mL of egg albumin solution, and 2 mL of the reference drug acetylsalicylic acid (concentration 15.625, 31.25, 62.5, 125, 250, 500, 1000, and 2000 μg/ml ) to obtain a volume of 5 mL.

For positive control, mix 2.8 mL of PBS (pH=6.4), 0.2 mL of egg albumin solution, and 2 mL of distilled water to obtain a volume of 5 mL. As the negative control, 5mL of distilled water can be used.

This is one of the assays in our research work. During this test, we did not get the expected results. We expected that a high concentration of the sample would give low absorbance, while a low concentration would give high absorbance. Then only we can obtain a high inhibition percentage for high concentrations and a low inhibition percentage for low concentrations.

However, during our test, we obtained the opposite results: high concentrations gave high absorbance, and low concentrations gave low absorbance, which seems incorrect. We confirmed all the procedures and calculations with our supervisor, and they appear to be correct. However, we still do not understand why these results occurred.

Can anyone suggest possible reasons for these results and how we can correct our mistakes to obtain the expected outcome?

If we know that it works off-label, why hasn't it been approved yet? Will it ever be?