Questions related to Drug Safety
We have proved that this plant has a such significant aphrodisiac effect on mature male rats, previously. Now, we're looking for tests that can be performed to look for the mechanism of aphrodisiac of the plant or any in vitro assays that can be used to prove the aphrodisiac attribution in lab. No more animals testing. Any input, dear scholars?
The solution in question is only slightly hyperosmolar - 315 mOsm/L.
I would like to conduct a clinical trial to do a head to head comparison between two drugs for safety and efficacy. How can I estimate the appropriate sample size?
Discuss the suitability of current regulations for biotechnology medicinal products globally under the following four topics:
(i) Fitness for purpose
(ii) Impact on, and response to innovation
(iii) Impact on the access of medicines to patients
(iv) Any other suitable topic(s)
You should provide, where relevant, examples and identify the regulations
I am conducting a research in drug-induced nephrotoxicity. In your opinion, what would be the most suitable standard to define drug-induced nephrotoxicity case? Is it KDIGO Clinical Practice Guideline for AKI or NCI-CTCAE v4.0? Or maybe you have another preference.
Please see the attachment for more details.
"For a topical solution drug product, in vivo bioequivalence may be waived if the inactive ingredients in the product are qualitatively (Q1 ) identical and quantitatively (Q2 ) essentially the same compared to the listed drug. In this setting, quantitatively essentially the same means that the amount/concentration of the inactive ingredient(s) in the test product cannot differ by more than + 5 percent of the amount/concentration of the listed drug. Where a test solution differs in Q1 and/or Q2 from the listed drug, in vivo BE may be waived, provided the sponsor submits evidence that the difference does not affect safety and/or efficacy of the product at the time a waiver is requested." Quoted from FDA draft guidance "Topical Dermatological Drug Product NDAs and ANDAs - In Vivo Bioavailability, Bioequivalence, In Vitro Release, and Associated Studies. The last sentence says that in vivo BE may be waived if Q1 and/or Q2 are different from RLD, but sponsor must submit evidence that difference doesn’t affect safety and/or efficacy. What are some examples of evidence that the FDA would be looking for to verify safety and/or efficacy?
I determined the cytotoxic effects of two drugs ( A and B, 24h, 48h, 72h). The concentrations of A drug was 12,5 , 25, 50, 100 µM and B drug was 0,1, 0,5, 1, 5 and 10 µM. I used excess over bliss calculator. However, I can not understand how interpret results? I added my results. Please, can anybody help me how interpret them? Additionally, I did not sure which analysis is the best? May I used IC50 concentrations rather than series of concentrations (A and B drugs)?
Condition Excess Over Bliss
It is becoming famous in some pharmaceutical industry that a raw material that is to be expired some few days maybe when discovered will be used for production of new drugs and the new drug will still be given an expiration date of 4 years.
Yes most times the potency of the drug is still 95 or 100%.
To avoid re-entrainment, the collection surfaces need to be coated with a suitale material.
I choose three coating matrials(glycerol coating, 1%Span in hexane ,1% Tween in EtOH) and uncoated cups to test, and having results between the four groups. But how to evaluate which one is better to my DPIs products?
ACE inhibitors are less efficacious and tolerant for African origin hypertensive patients.
Does anyone know the molecular mechanism behind this? i.e is it related with low rennin release or beyond?
When estimating EC50 for a single drug, does one need all of the raw data at each drug concentration or simply the average response at each concentration? How does one decide what model or equation to choose (e.g. four versus five parameter logistic curve)? When obtaining the EC50, is there a best approach for determining the 95% confidence interval?
When choosing the concentration of a drug for an experiment you look at the EC50 of that drug and use 10xEC50 to make sure you get an activation of the receptors you are interested in... However i don't understand how you get that value and whether it is subject to change under different conditions. What are the parameters that determine the EC50 of an agonist (in this case CHPG)? Does it change from one cell type to another or between different preparations? If so, why?
Isolated studies have proven superiority of this combination over plain aspirin in reducing gastric disturbances. The FDC of low dose aspirin and glycine is approved in India. However, data on its efficacy, safety and comparison with enteric coated aspirin is sparse.
I have very limited therapeutic options treating a patient with extensively Drug resistant TB. However there is no evidence in the literature of the association of these two drugs in a regimen. They are now commercially available however there is little consensus to adding them together given the paucity of safety data. Has anyone managed to give the two drugs together, where there any adverse events and/or increases in QTc?
Dear Dr. Piccini and colleagues,
Many thanks for sending e a full text version of Paraesthesia after Local Anaesthetics: An Analysis of Reports to the FDA Adverse Event Reporting System. It is a very important work.
You may be interested in my continued research subsequent to my 2006 paper that you kindly referred in your article.
If you send me your e mail address, I would be more than happy to send you my recent works, a combined clinical- and registry study, and an animal experiment.
Søren Hillerup, PhD, Dr Odont.
Professor em., Maxillofacial Surgery
Should patients be able to choose whether they are given treatments that have risks, if they are told what the risks are? In relation to macular degeneration, the trials into stem cells as a cure won't be offered to patients for a very long time, even though it is very promising. Patients that are currently suffering from the condition will have irreversible damage to their eyes before stem cells are offered.
With the concern over adverse side effects of synthetic chemicals, millions of people across the world are turning back to plant derived healthcare and other products. The world market for such products including pharmaceuticals, nutraceuticals, fragrances, flavours, biopesticides and colour ingredients, alone exceeds several billion dollars per year. However, the major challenges in this sector are with the overall quality, safety and efficacy of these products. The claims and other information provided on the label may be far from what is in the pack. Just because an herb is natural does not mean that it is safe. Nevertheless, if herbal products are to assume a respected place in the market and society, more reliable and credible means and ways as well as greater authoritative regulatory directives for quality and safety of the herbal products are warranted. In this context, the question is to what extent the existing scientific standards and regulatory norms are adequate and effective for ensuring the quality and safety of herbal products?
My question does not just refer to their commercial use but also the R&D one… Let’s say I want to submit a Horizon 2020 project for a nano-functionalized cosmetic crème (not a medical grade one), would I still have to foresee clinical trials?
Does anyone have any experience on the EU’s ethics guidelines on this point?
This question is related to HIV drug class called fusion inhibitors. There is only one Fusion inhibitor called T20 (Enfuvirtide) approved by the FDA. I couldn't find the exact reason why the Roch and its partner company halted the development of T1249 in the middle of Phase II clinical trials despite of having good results!
In India there is no requirement of proving BE study. Dissolution studies are sufficient. Should there be strict implementations of BE studies be made for registration of ANDA for marketing in India?
I'd especially be interested in systematic review-type information, but equally happy with data from sizable, well-run one-off studies.
There is well-established literature on the safety and efficacy of drugs like Atorvastatin Vs Rosuvastatin, Phenytoin Vs Carbamazepine etc. Is it necessary to compare again and know the safety and efficacy of such drugs in a hospital set up, despite of well established scientific literature?
In my daily practice, I have seen many people reporting ADR's without a causality assessment and even few were reported without clinically observing the patient. Is this appropriate? How do we overcome these obstacles for better results? Please help the reporters in overcoming such barriers with your suggestions.
Most observational studies on community-acquired acute kidney injury use hospital admission and relevant ICD codes as their study outcome. However, we have access to a primary care data base that can be linked to laboratory data and this may allow us to additionally study renal outcomes that did not require hospital admission and those that were not primarily attributed to AKI.
Seeing first hand all the different reactions patients have to medications and how these reactions can differ wildly when using the generic version of a medication. How can a medication be called a generic version if the adverse events experienced differ so much from the original medication? Could this be due to the other agents present in the medication and not the principal agent itself?