/r/pharmacology
News, peer-reviewed academic articles, and discussion of pharmacology & toxicology, with a particular focus on new drugs.
News, peer-reviewed academic articles, and discussion of pharmacology & toxicology, with a particular focus on new drugs.
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/r/pharmacology
I’m working with a psychiatrist and he’s interested in writing a paper on a patient who claims to use this drug, however he couldn’t find what lab tests for it (and has since tasked me for finding where to test it). I tried my universities test directory, and other major hospital test directories in my region, but couldn’t find anything.
Where would I look next? I also just tried Google “4-Fluorophenibut test” and other related terms, but still didn’t find anything. It looks to be a pretty rare drug, so not a lot of relevant literature on it either. Is there a center I can call, where they would know where to order a test from?
Is the sleep disturbance caused by melatonin suppression when taking beta blockers only an issue when the beta blockers are in effect (such as the 4h time for 10mg Propanolol dosage), or can it cause disruption regardless of what time of the day they're ingested?
I’m not looking for basic PK like on coursera but a full PK course that’s 10 hrs or longer with calculations. Thanks!
Just a bit curious. I'm a layperson with no formal education, so if these are bizarre questions or if they're just making bad assumptions, I apologize.
Reading about a number of drugs like monobenzone, doxorubicin, apap, etc. that undergo redox cycling after seeing it in a book. I read a paper about treating melanoma with 4-(4-Phenylbuta-1,3-dienyl)benzene-1,2-diol, which is similar to monobenzone in that it goes through tyrosinase to form a quinone, which can deplete glutathione below a critical level and kill the cell. How can I find more information about what enzymes catalyze what reactions, and how the backbone of a compound can change that despite having the same functional groups?
I've read monobenzone can also haptenate proteins. Other than for treating melanoma or vitiligo, what other drugs undergo redox cycling in a way that is therapeutic or contributes to side effects? If they can seemingly constantly regenerate, how does that process finally come to an end?
I'm looking to get my PhD in Pharmaceutical Sciences. When looking at school rankings, I'm having a hard time figuring out how these programs specifially ranks. Should I be looking at Pharmacy School rankings, which is where this PhD program typically is located, or should I be just look at PhD in Pharmacology rankings? I have noticed some similarities in these rankings, but also a lot of differences so I wasn't sure.
Hi, I have been working in clinical research as a CRA since graduating undergrad 2 years ago. I feel stuck and have been thinking of career changes, but I’m not sure where to begin. Where has your pharmacology background taken you?
I’ve been curious and unable to get an answer to the following question on several other Reddit subs, so I thought I’d post it here.
Clonazepam is a nitrobenzodiazepine, and as I understand it, a chlorinated analogue of nitrazepam. As such, would the chemical name “clonitrazepam” be just as correct?
It would seem, following other patterns of benzodiazepine chemical names, that clonitrazepam would be more accurate. Perhaps clonazepam is what was chosen and is just slightly truncated for convenience?
I’m currently debating between pharmacology or pharmaceuticals science… but I was wondering if I did a master, get an entry level job and do a part time PhD, would that be wise?
Also I’m conflicted between the two based on salary at the end of the PhD. I love researching the effects of drugs and also heading towards wanting to eventually develop drugs (still debating). What would you advise has a better “return of investment” with career and salary?
if I did a part time PhD, I could also work part time im assuming? I wouldn’t want to do a full time PhD just because of how low stipends are and would love to gain experience in the field before/during it.
So I read that IC50 is the concentration of the drug which reduces the maximum response is reduced by half. But I was wondering how this reduction happens(in other words what type of drug would be relevant here). I’m guessing antagonists? Perhaps partial agonists or inverse agonists as well? As these types of ligands will shift the conformation state of the receptor from active to inactive
This might be a really stupid question. I'm taking a pharmacology class and my professor uses "absorption" to mean the passive diffusion or active transport of a drug across a cell membrane. She seems to delineate water solubility (and therefore ionization, H bonding) and absorption as two separate, inversely-related things. She has also mentioned how absorption directly influences pharmacological activity; this confuses me, however, because if that's the case, then why would absorption across cell membranes matter for a drug whose target is a cell surface protein, like GPCRs? This question is particularly breaking my brain. Is she specifically referring to absorption across the gastric epithelium, and then into the bloodstream? If that's the case, then how does that logic still apply to other routes of administration like IV, where it's delivered directly into circulation? Thank you for any help. I think I may be overthinking this.
Hello everyone. So the textbook "The pharmacological basis of therapeutics" states:" With first- order kinetics, clearance CL will vary with the concentration of drug (C), often according to the equation: CL=Vm/Km+C , where Km represents the concentration at which half the maximum rate of elimination is reached (in units of mass/volume) and Vm is equal to the maximum rate of elimination (in units of mass/time)." How is this a first order kinetics equation ? I thought clearance remained constant regardless of drug concentration in first order kinetics .Thank you in advance for answering.
ammonia chloride is commonly used for amphetamine overdose since it can acidify the basic drug but I read that it isn't used clinically due to its potential to easily produce toxic acidosis. Does this mean it has a low therapeutic index?
Hello!
I recently learned about suboxone and methadone in my clinical medicine class, but still feel like I don’t have a great grasp on it. Can someone please tell me the difference between suboxone and methadone besides suboxone having a ceiling effect and being a partial agonist while methadone is a full agonist, and that methadone is administered by an opioid treatment center while suboxone is prescribed? Also are both of these drugs forbidden to be taken by individuals with certain occupations, ie pilots? Any additional info you think would be helpful is greatly appreciated!
Thank you!
Hi I just started a new course in pharmacology but I realized I lack a lot of pre-requisite knowledge for calculations and I’m stuck on converting DPM to mol. I’ve attempted it but don’t think I’ve done it correctly yet. I first took the DPM and divided it by 2.22 x 10^12 to give me the value in Ci. Then to gain moles from the Ci I divided the Ci value by the specific activity to give me the value in mmol. Is this correct? Thank you :)
Pharmacology student here. I have been giving this data set from a saturation ligand binding study and need to produce a scatchard plot. Can anyone explain to me why the first row of data reads 0 and if I am okay to plot this but essentially ignore it when drawing a line of best fit.
The reason I ask is if I ignore the 0 when creating the straight line it almost perfectly matches my Kd and Bmax values for the nonlinear curve graph I’ve already done. But if I include the 0 it distorts it quite heavily and it is wildly different.
If I can’t ignore the 0 can someone give me an explanation I can write as to why the values from the 2 different graphs differ?
Thanks!!
Hello! I'm a first year medical student and have a pharmacodynamics-related question. In the context of non-competitive antagonism, what happens to the value of EC50 in the presence or absence of spare receptors? Some resources say it remains unchanged, while others say it will either increase or decrease. My lecture slides say that EC50 will increase in both the presence and absence of spare receptors but that does not make any sense.
Hi, med student here.
I came across some plots from this article. Unfortunately, I don’t have access to the full version, so the answer to my question may be in there.
These plots show a linear dependence between urine flow (X-axis) and renal clearance (Y-axis) of ethanol and butabarbital. In the case of urea and chloramphenicol, the function is represented by a branch of a hyperbola.
I don’t understand the kinetics in the case of urea. Since urea reaches the lumen by passive diffusion, I would have expected a linear relationship without a plateau. Additionally, considering the reabsorption process, I would have expected a slow increase in clearance at low urine flow due to the higher gradient between the lumen and the plasma.
Where’s the snag?
Hi! I am a Pharmacist in working in R+D of generic drugs. Just wondering if there's any Regulatory Affairs Specialist from the EU (Including the UK) here to make a question about References medicines. Is there an official list with the reference drug for a medicinal product like the FDA's Orange Book (The reference drug is called Reference Listed Drug or RLD). The request is because I need resources to create protocols for Bioequivalence studies (in vivo and biowaivers). I've been looking for this but no result, also I verified in the EMA page and other agencies.
Thanks in advance.
Hello Everybody! I'm currently a High School Senior in the States looking to get into Pharmacology. I was fortunate to get a job as a pharmacy technician for the past year and have fallen in love with the field. Specifically, how medications work and affect the body. However, I also witnessed how exhausting retail pharmacy can be, especially for the pharmacists. Currently, I'm in between Pharmacy(Hospital or residency) and Pharmacology but feel I don't know enough about the Pharmacology pathway.
First, what's the career like for a pharmacologist? Is it purely in a laboratory setting or are there other workplaces available? I've also seen a lot of programs offering what is pharmacology/toxicology. In the workplace, is there a major difference between the two?
Second, can you specialize in a specific field in pharmacology? Can you specialize in something such as neuropharmacology? Would I need a degree in neuroscience as well? Any recommendations for an aspiring pharmacologist going into college?
Hopefully this type of question is allowed here and I appreciate any info or answers!
Hello, my bachelors was in biological anthropology, and I’m currently a biomedical anthropology MS student working in a lab in the pharmaceutical sciences department at my current university in addiction genetics with mouse models. I was wondering if anyone has:
My shortlist I’m considering are:
I originally had UWash, UBuffalo, and Northeastern on the list, but have personal considerations for cutting them. If someone convinces me that my considerations are lesser than the pros, I might apply.
Hi all
I’ve completed my BSc in Pharmacology and my career aspiration is to become a patent attorney within the pharmaceutical field.
I’m going to do an MSc next year but unsure which MSc course to do. Are there any fields within life sciences that you think there will be a strong demand for patent attorney’s in the future? Or MSc’s that will make me an attractive candidate for training contracts?
I’m currently looking at MSc’s in Pharmacology, Immunology, Virology, Stem Cells and Neuroscience.
TIA!
I will be completing my MBBS next year, but instead of pursuing clinical specialties to work in a hospital setting, I am passionate about pharmacology. My goal is to either become a professor in this field or work in the pharmaceutical industry. However, I have realized that many advanced pharmacology programs require a background in mathematics, which I did not focus on during my undergraduate studies. I am seeking guidance on how best to bridge this gap and fulfill the necessary requirements. Specifically in the USA
Hello all, My name is Adrian. I am currently a high school senior currently applying early to colleges.
I am aiming to be a Pharmacist and am trying to set myself up with a solid undergraduate education. I consider myself a fairly versed student as far as my education. The math/science courses I have thus far taken that I would view as concerning pharmaceutical studies are Biology Honors, Geometry Honors, Algebra Honors, AICE Environmental Science, Pre-Calculus Honors, Forensic Science, Chemistry Honors, and I am currently taking AP Biology as well as Calculus Honors.
My biggest concern is in majoring in biology which I had my heart set on for a little bit now due to my interest in the subject as well as the direct correlation it has to my desired career. The problem with biology is that it is highly regarded as one of the hardest majors, though I most definitely see myself as capable (as I am a firm believer that I can do anything I put my mind to), I wonder if I am setting myself up for an unnecessarily stressful undergraduate life. My second choice is to major in psychology which is another longstanding interest that I have had (specifically forensic psychology) and then taking the classes necessary for pharmacy school.
I guess what I need clarity on is:
Is majoring in Biology as hard as it is chalked up to be?
Does majoring in Biology seem reasonable/feasible for me given the courses I've taken (feel free to ask follow-up questions regarding specific grades, my GPA, etc.)?
If you are familiar with pharmacists who majored in Biology how important is it for success in Pharmacy school as far as preparedness (I imagine it isn't integral to success, but did they have a significant edge over those who didn't)?
Thank you in advance for your help and guidance and please feel free to let me know if you have any more advice on the admissions process or anything else you feel may be relevant!
Beloved swarm intelligence, I am currently looking for in vitro and in vivo possibilities to evaluate the impact of a drug on mucociliary clearance. So far the only in vitro assay I found is provided by Epithelix. There are some possibilities in vivo, from measure particle to phenol red clearance. Are there any people out here with experience in any respective in vivo assay, possibly with a recommendation for a CRO offering the assay?
Pramipexole is given as an adjunct alongside irreversible MAOIs. As the title says, why, if mono amine oxidase is being inhibited, would it not affect the production of dopamine in the mesolimbic system from D3 agonism?
I'm a certified pharmacy technician and working in retail pharmacy is absolutely horrible. both the technicians and pharmacists are yelled at daily and I just can't take it anymore as an introvert and as an autistic person.
I absolutely want to stay in medicine but be more into a lab setting where I don't have to interact with the public every single day.
Is pharmacology good for introverts?
I have a question regarding a statement in this article:Toutain PL, Bousquet-Mélou A. Volumes of distribution. J Vet Pharmacol Ther. 2004 Dec;27(6):441-53. doi: 10.1111/j.1365-2885.2004.00602.x. PMID: 15601439 If we assume that no drug has been distributed,then why isn't the concentration fixed since the whole drug is in the blood and the plasma concentration is known(say we have calculated it somehow) I tried explaining this by assuming that the text means no further distribution after a hypothetical instant distribution of the drug,but I'm not confident in this assumption. Thanks for answering in advance .
Hello! I have a question regarding a case study. The patient’s empirical treatment plan lasted for 6 weeks. During the first 2 weeks, she was on a triple therapy consisting of amoxicillin, clarithromycin, and omeprazole. While taking these medications, she discontinued both simvastatin and ibuprofen. After completing the antimicrobial treatment, she resumed taking simvastatin and ibuprofen for the remaining 4 weeks. Why was there a need to stop these medications during the initial phase of treatment?
Additionally, as this regimen eventually proved unsuitable, her omeprazole dose was adjusted to 40 mg once daily, whereas previously she was taking 20 mg twice daily. How does this change affect the pharmacokinetics of the drug?
Hey Everybody!
I've been extremely interested in entering the pharmacology field, and was wondering what undergraduate degrees would get me on track to entering a pharmacology program in the future. I figured it would be best to ask those that have already studied or are currently studying as you often have different insight after going through the experience yourself.
Thank you in advance for any responses, I truly appreciate anyone that takes the time out of their day!