Talk:Atorvastatin

Generic versions of Lipitor

Why are generic names of Lipitor not allowed on the atorvastatin calcium page? Is this page owned and controlled by Pfizer, the drug's maker in the US. Generic drug names such as Lipvas and Atorlip are approved and completely legal brands made by well known international drugmakers and sold by pharmacies in the US and worldwide. Why is this page so US-focused and the public not provided this helpful information? Has Wikipedia adopted a NO freedom of speech policy? By having access to these generic names and knowing their options, consumers can get the information they need and potentially save hundreds of dollars monthly on their drug expenses if paying out of pocket for their expensive medications.

User:Mykjoseph1958 (talk)

The genric name is atorvastatin. The brand name is Lipitor. Lipvas and Atorlip are not generic names, they are brand names. Lipvas for example is the brand name of Okasa Pharma, of India.

WP entries use the generic name of drugs. We also add the brand name because it is more familiar to many readers. We had a long discussion about that on WP:MEDMOS.

I agree with you that consumers should have access to information about generic drugs. I posted a link on the Statin entry to Consumer Reports Health.org which explains when generic drugs are better.

The test of whether to include something in an entry, in my opinion, is whether it makes it easier for the reader to get the information that he or she wants. Having a long list of brand names in the introduction makes it hard for a reader to get through it. If we do have a list of brand names, it should be further down. In some cases (such as aspirin or penicillin), a drug might be sold under so many names that listing them all would make the article difficult to read.

Furthermore, this is the English language Wikipedia, so you'd have to make a good case for including brand names that aren't used in English-speaking countries.

I think that's a reasonable position. Does that satisfy you? Nbauman (talk) 02:25, 7 January 2009 (UTC)

Drug Interactions

Atorvastatin is one of the most widely prescribed drugs in the statin class and on the market and one that interacts with numerous other medications. Take a look at other drugs like prozac, alprazolam, flouroquinolones, etc. Virtually all drugs currently have some section for their interactions and with one that interacts with so many other common medications it is a severe deficiency to completely ignore them. Clinically speaking interactions are the second most important factor with respect to the drug, if you are going to have a page that includes the pharmacology and indications it seems completely contrary to then exclude the interactions. By that standard most of the information on the page should be removed.

The official label for this drug is 51 pages so having a couple paragraphs on it is hardly a verbatim copying of the "package insert".

Separately I have a hard time understanding why there is such reluctance to include more information from the official FDA drug label, at least to the extent that it is summarized, that data is not represented well online and is a conclusive and legal regard approved by a panel of relevant experts which seems to meet exactly the definition of encyclopedic in the wikipedia guidelines (though obviously those are open to interpretation). In the US that FDA label is the only statutory authoritative reference regarding the drug.

Is there any form of representing the interactions you are comfortable with? Pinetop18 —Preceding undated comment was added at 09:13, 29 January 2009 (UTC).

GA Review

This review is transcluded from Talk:Atorvastatin/GA1. The edit link for this section can be used to add comments to the review.

This article does not meet the good article criteria and has too many issues. It has therefore failed its nomination. Issues include but are not limited to:

• Insufficient references. Some sections are nearly completely uncited, such as "Pharmacokinetics".
• There are several citation needed tags.

Questions and comments placed on this page will receive responses. Once these issues have been resolved, feel free to renominate the article. Thanks! Gary King (talk) 19:03, 7 February 2009 (UTC)

Stroke and HDL

I might as well open the discussion here. Eddievos (talk · contribs) added information on the influence of atorvastatin on stroke risk and HDL levels. I removed this for a number of reasons:

• No actual references were provided (only the names of the trials)
• The data are cherrypicked from trials, rather than sourced to review articles (see WP:MEDRS for the importance of this)

This needs to be discussed properly. JFW | T@lk 15:10, 15 February 2009 (UTC)

Response

Response by eddievos, hoping this is the correct location to do so:

The 1st paragraph states that atorvastatin reduces (generic) stroke without reference. The (stroke focused) study that showed it reduced transient (TIA) and clotting strokes was SPARCL (vs placebo} but that study also showed an over 95% probable significant increase in bleeding strokes and that should be specified in the introduction. Bleeding strokes are the most deadly and debilitating of strokes and there is evidence [an observation by the SPARCL authors] that RECURRENT bleeding strokes are promoted by atorvastatin [factor >6]. I would be glad to add Medline references to these major studies if that would help-and some are already there. In the mean time, the statements that are currently there should be clarified and properly referenced.

Also, there is no reference for the idea, presented as fact, that atorvastatin "stabilizes plaque", a concept commonly thrown around as established fact but that has not been shown to be accurate in human studies. For example, since plaque rupture may cause myocardial infarction of which a significant percentage (>/=20%) is a fatal event, the certainty that no statin has EVER lowered mortality in women according to 2 meta analysis [JAMA and JACC] and the fact that the flag ship atorvastatin study, ASCOT, ended with overlapping mortality curves [as have its -only- 2 other major placebo controlled studies, ASPEN and SPARCL] and a 49-in-house study combining study by atorvastatin's maker have shown no difference in mortality. Moreover, ASCOT found 2 more "events" in women at study end.

This is not opinion or cherry picking of studies, this failure to lower all-cause mortality in our top killing disease is THE hardest non contradicted all-study result regarding atorvastatin, and it is incorrect that a modification of the text reporting this is simply removed.

SECONDLY (line 73): it is incorrect to suggest that atorvastatin raises HDL because atorva is virtually unique among the statins with the property that it does not raise HDL.

THIRDLY, there is bias or at least 'slant' in the suggestion that atorva+ezetimibe lowers LDL more "effectively" [suggesting benefit] than the combo of simvastatin + ezetimibe. The correct wording would be "to a slightly greater degree". The latter drug combo ended in the failed (surrogate endpoint) ENHANCE study, and I had the pleasure going to ACC 08 in Chicago to assist in the revealing of the results, and there is no indication that the cited combo of atorva + ezetimibe is "effecive" in any health endpoint; some of those studies are underway and nobody can guess the future outcomes that may be no or greater mortality. Eddievos (talk) 19:17, 15 February 2009 (UTC)EddieVos

Misleading passage

Citing this form the opening paragraph: "It also stabilizes plaque and prevents strokes through anti-inflammatory and other mechanisms."

The drug itself does neither. Evidence shows that reduction of total cholesterol may lead to plaque regression, but it is not a mechanism of the drug and is by no means guaranteed. Second, it has absolutely no anti-inflammatory mechanism.--Mrdeath5493 (talk) 08:04, 24 February 2009 (UTC)

---

response by EddieVos: you're absolutely right and there are 2 studies showing that calcification of the artery [Medline 16415377] and of the valve of the aorta [Medline 15944423] continues unabated regardless the atorva dose or placebo; when calcification goes on, what is stabilized?

However, as long as Dr. JFW controls this page (like all other statin pages he started) there will be blanket supportive statements based on single studies [ref's 17, 18] or drug comparative studies [the next ref, #19] while studies that found no benefit in this case in diabetics [for example: the original ASCOT and ASPEN studies] have no place, and 'independent thought' is not allowed in Wiki [mostly with good intent and reason].

ALL atorva/Lipitor studies ever done were manufacturer supported, and NONE of them show a mortality benefit in anybody vs placebo, what is the chance that Pfizer will pay for a meta-analysis [Wiki's preferred proof] saying that will ever see the light in a journal publication? When I say this on this Wiki page, the page controller JFW simply undoes the edit. Interestingly, it was the C.E.O. of Pfizer who instructed the man in charge of arorva/Lipitor to release the mortality data of their 49 in-house studies to me, and they were not supportive of benefit [placebo did better but, like any other study, it did not reach significance].

The same consensus problem [undo] applied to a supposedly FDA sanctioned HDL raising effect of atorva that does not exist (and high-dose studies show that atorva lowers HDL) but clearly Pfizer would rather pay to NOT have those hard facts published in a comprehensive Wiki-acceptable format, and it has not been so reported.

Here we have the top selling drug on the planet that people will visit Wiki for, only to find one sided, technical or irrelevant data [Dr. Jarvik's halted ad campaign] yet there is nothing that tells them how Lipitor[TM] will help them, and where it will not help or even hurt them. Billions $$ worth of research, a true treasure trove, but it's all single study so far and cannot be reported in Wiki. Clearly Dr. de W, the statin pages you fathered need to be improved with balance. I know the consensus ATP III opinion about statins but the authors have 10 [ten] pharma conflicts each, in the U.S., and almost that many in Canada. Does that merit Wiki status? Tell us how debate on this page will help establishing statin reporting balance. vos{at}health-heart.org —Preceding unsigned comment added by Eddievos (talk • contribs) 15:06, 24 February 2009 (UTC)

I will continue to "control" the page until you stop cherrypicking the studies and base your edits on sources suggested in WP:MEDRS. JFW | T@lk 00:28, 26 February 2009 (UTC)

Side Effects

What side effects does the drug have? —Preceding unsigned comment added by 80.94.32.80 (talk) 14:47, 3 March 2009 (UTC)

More from Mr Vos

Mr Vos (see above) emailed me to ask whether I would "permit" the insertion of the following two facts:

• Atorvastatin does not decrease mortality
• Atorvastatin does not increase HDL

Now as I have tried to explain several times now, it is not that these facts can or cannot be cited, but the fact that we need good sources for them. Statins don't normally raise HDL, because they don't interfere with that process. With regards to mortality, it would be good to cite a source that says so explicitly. On the whole, statins do indeed have a mortality benefit (overall and cardiac mortality) - http://gut.bmj.com/cgi/content/full/58/4/473.

Now please tell me why atorvastatin is so deserving of your attentions. Do the same issues not also exist with the other statins? Or is it just that atorvastatin is so popular in the USA and Canada? JFW | T@lk 01:48, 14 April 2009 (UTC)

Thank you JFW for the creative comments. Your link went to GUT, the Journal. Why atorva/Lipitor? Well that is the subject and it is arguably the statin with the most massive study base [and in the U.S., once most advertised]. I shall try and obtain a combo source that confirms from several studies that atorva has no mortality benefit, something evident for anyone looking at the mortality curves from ASCOT that never separate and a study that ends with 2 more cardiac 'events' in women. Regarding women, there are 2 meta analysis that conclude about statins that women have no mortality benefit (Wiki worthy evidence, but not specific re atorva) http://www.ncbi.nlm.nih.gov/pubmed/15138247?dopt=Abstract [JAMA 2004] http://www.ncbi.nlm.nih.gov/pubmed/15337211?dopt=Abstract This is Wiki acceptable evidence, but not specific re atorva, and could be said on all statin pages regarding women with or without heart disease: they don't lower all-cause mortality. I'll wait for your proper reference regarding male mortality; regarding patients over age 70: PROSPER was conclusive that there is no all-cause mortality benefit.

Agree, statins (except rosuva/Crestor) don't raise HDL and atorva may even lower it. So, why cannot I/you remove/alter that phrase from the supposedly atorva FDA list of actions (item 1) unless it is specidied to only apply to patients with "isolated hypertriglyceridemia", whatever that is in real life; it DOES NOT apply to 99% of those enrolled in trials, less the public.

Finally, regarding the stroke issue: SPARCL showed an INCREASE in bleeding strokes that was significant; that trial was in stoke victims, it showed harm and why cannot that be said for balance? regards, E. Vos vos@health-heart.org —Preceding unsigned comment added by Eddievos (talk • contribs) 09:30, 14 April 2009 (UTC)

Could you try to thread your discussion posts as shown above? The link was indeed incorrect. The correct link is http://archinte.ama-assn.org/cgi/content/full/159/15/1793

"2 more cardiac 'events' in women" may be a correct number, but you are not telling us the statistical significance of that number. The result from SPARCL was an outlier and that's probably why this "evidence of harm" is not widely quoted.

You can continue muttering about all-cause mortality, but I would argue that significant event reduction is a worthwhile endpoint. Being admitted to hospital is an unpleasant experience, and recurrent cardiac events will eventually leave the patient with ischaemic cardiomyopathy. JFW | T@lk 22:30, 16 April 2009 (UTC)

Forgive me JFW for not knowing how to "thread" a response, and for what you call "muttering" about mortality.

Regarding women on Lipitor/atorva in ASCOT: the 2 more events at study end were obviously not demonstrated harm but it showed that when you start 979 women for 3.3 years on atorva, you may end up with 2 more 'events' vs. placebo, i.e. no treatment benefit which is the purpose of taking a cardio prevention drug. From the Lancet 2003 text: no significant benefit in 6 sub-groups and "no benefit was apparent in women. Put another way: you can have 3200 women with minimum 4 risk factors for heart disease spend $m3 for that drug and have zero possibility of ANY benefit. Ditto for diabetics.

Did you actually study my hyperlinks above regarding women and mortality? There is zero chance women will live longer at any risk level. 3 reasons people take statins: fear of death, fear of cholesterol or fear of displeasing doctor. Reason 1 is THE motivator and is not "muttering" but vital endpoint, and should be dealt with on Wiki re statins.

Regarding SPARCL in post (ischemic) stroke patients, here http://www.neurology.org/cgi/eletters/68/10/719#7946 is yours truly with a Dutch cardiologist elucidating results. This is THE standard study in stroke/statin. In May 2009 LancetNeurology by SPARCL authors: "we recommend caution when considering statin in patients with prior cerebral haemorrhage". That is not said in the opening paragraph of the Wiki text.

Re the PDF of your 1999 meta-analysis: no average duration for NNTs is given, women are not mentioned and EXCEL study excluded [RR for death +2.75 P=.11]. Interestingly and logically, the best effect is in angina (and resulting non fatal MI's recorded) and that may just be from the NO/eNOS effect of statins where nitroglycerin is safe and effective (ref. http://www.ncbi.nlm.nih.gov/pubmed/12634978?dopt=Abstract ) Conventional wisdom has it that when a therapy to obtain a clinical benefit costs over $50,000 it is not cost effective in Western societies and no endpoint for statin in that meta-analysis even comes close. Said another way, all endpoints are well over 100 on-drug patient-years, in women on atorva 1000's of years and ditto for TIA + ischaemic stroke.

Your point of recurrent 'events' leading to 'ischaemic cardiomyopathy' may seem logical but there is zero evidence that statins prevent any form of cardiomyopathy [think: rosuva in CORONA/Gissy-HF].

Question: heart disease killing millions of people, how come then that the FDA's of no country has allowed the claim that any particular statin extends life? Answer: they don't in any but the most unusual group of male patients, for limited amount of time, and at astronomical cost per life extended. Atorva never did/will at any dose extend life. Eddievos (talk) 13:32, 18 April 2009 (UTC)

Original research?

I am assuming good faith. Can someone please explain to me why the effectiveness of the drug, from a report Pfizer published themselves, that has been further reported by mainstream media and other medical professionals, is original research? Freikorp (talk) 02:35, 26 February 2010 (UTC)

This of course is the report from Pfizer I am talking about [1]. Get a calculator, crunch the numbers. articles.mercola.com/sites/articles/archive/2008/05/08/medicine-s-dirty-little-secret.aspx?source=nl [2] Freikorp (talk) 00:23, 27 February 2010 (UTC)

The fact that you expect me to "get a calculator" shows where the problems lie. I know the Business Week article. It happens to focus on Lipitor, but it is actually more concerned about primary prevention with statins as a whole. It is a rubbish article: it doesn't even bother citing the ASCOT study by name, even though much of its arguments hinge on interpreting that trial's endpoints. I will not waste my time critiquing Mercola; he's not a reliable source on medicine (plus, the site expects me to register).

You are probably correct that WP:NOR was probably not the predominant problem of your contribution (although WP:SYNTH might be). There are some perfectly useful reliable sources that make exactly the same argument. Some of them are even cited in detail on statin. Have a look there. JFW | T@lk 06:22, 28 February 2010 (UTC)

Thanks for bringing WP:MEDRS and the references in the statin article to my attention. I'll take this information into consideration before making further contributions. Freikorp (talk) 07:17, 28 February 2010 (UTC)

Hatnotes

SlimVirgin (talk · contribs) added a hatnote pointing to the statin article, suggesting that this may be necessary to direct users there. I reverted this addition because it does not, in fact, disambiguate the article title (Atorvastatin is fairly specific) and therefore seems not be useful according to WP:HATNOTE. The hatnote was reinserted because HATNOTE does not explicitly counsel against such use of hatnotes. I think it does. WP:RELATED, WP:NAMB are two examples that seem to touch on the situation here. Again, as I said in my edit summary, the concept statin is mentioned in the first sentence, and I can see at least one further instance of {{Main}} where relevant. I suggest we drop the hatnote, but I will refrain from doing this until SlimVirgin has had an opportunity to respond here. JFW | T@lk 19:10, 23 August 2010 (UTC)

I agree, for the reasons outlined below. Fvasconcellos (t·c) 20:08, 24 August 2010 (UTC)

Cross-posted from User talk:SlimVirgin.

Again, a question: do you understand why a hatnote is unnecessary in Atorvastatin? Fvasconcellos (t·c) 21:59, 23 August 2010 (UTC)

I would like to draw attention to it, and the hatnote helps to do that. There are millions of readers on this medication, some of them looking here for information about it. Our articles about it are terrible and hard to navigate for people without medical knowledge, which is who we write for. I am trying to make it a tiny bit easier for them to find the general article. Why would anyone object to that? SlimVirgin ^{talk|contribs} 22:03, 23 August 2010 (UTC)

Because it is completely unnecessary (see WP:RELATED). (A) The first line of the article says "Atorvastatin (Lipitor) is a member of the drug class known as statins". Reaching the main article is as simple as clicking on "statins", and there's no need to say "This article is about Lipitor"—the lead says so! It's redundant. (B) The articles are terrible now; hopefully, they will improve soon. As the statins are a pretty homogeneous class of drugs, articles on individual statins should obviously include some general information as well; that's a straightforward content addition. If that's not enough, Main article: statin can be added to relevant sections. Don't underestimate the intelligence of the general readership. With all due respect, this is a prime example of "dumbing down", not "making it easier". Fvasconcellos (t·c) 22:12, 23 August 2010 (UTC)

Generic statin indications, effects, contraindications etc

I think it is really hard to manage all this aspects updated across all statin related pages, would not it be more useful to link to statin page and only explain where significant differences exist? Richiez (talk) 08:32, 20 September 2010 (UTC)

I have a better idea. Link to the common or significant AEs from the product insert and from secondary sources, and dump the rest. Most statin AEs are class effect related, but we must presume that each molecular entity has its own profile. JFW | T@lk 10:44, 20 September 2010 (UTC)

At this point I am more concerned about keeping the ever changing lists of indications updated than AEs. For AEs it makes more sense to treat each product specifically, but the indications as far as supported by hard evidence are almost always linked to generic effect (even if it is present at different "strength") and not some peculiar properties of a special product. Also it is fairly rare that substantial new information on AEs emerge while information on indications is changing faster than I can read it. Richiez (talk) 12:44, 20 September 2010 (UTC)

This sounds like a discussion we ought to have on WT:PHARM. On the whole, lists of AEs shouldn't need to be "ever changing". When a drug is marketed, common AEs are already well known. It is only the rare ones that cannot be found until post-marketing, because no drug company can design a trial large enough to capture rare events. JFW | T@lk 00:20, 21 September 2010 (UTC)

re AEs exactly my opinion. Most AEs are known since decades.. most benefits also. What is changing rapidly and needs constant attention is the ever developing opinion on the tradeoffs of efficiacy, cost effectivness and safety for particular patient groups and indications. Every new trial adds some new information about this tradeoff and usually if it is shown that one statin improves 5 year survival of women age 65-70 with or without previous CHD and 5y followup this is interpreted to be applicable to generic statins. This is arguably incorrect but survival benefits are to a high degree sensitive to age and gender and for some genders and age group combinations there is no better data. Much of this data comes from meta analysis mixing trials on different statins anyway (and presumably trying to ensure these are reasonably homogenous) so it would be more appropriate to track it it on the main page. Richiez (talk) 09:25, 21 September 2010 (UTC)

With regards to the cost-benefit ratio, we should really only base ourselves on WP:MEDRS-compatible secondary sources for such information. Sources that put those individual trials in context, in other words. JFW | T@lk 09:41, 21 September 2010 (UTC)

I would go even further, we should keep anything that is not atorvastatin specific (also for AEs) at absolute minimum. Richiez (talk) 18:15, 21 September 2010 (UTC)

Single dose?

I've seen some Statins given as a STAT dose. Any medical explanation?! --Roomstop (talk) 23:58, 10 March 2013 (UTC)

Depends on the circumstances, but there is some data from TIMI that loading with high-dose atorvastatin can improve prognosis after MI. JFW | T@lk 21:52, 13 March 2013 (UTC)

There is some evidence that a single high loading dose of atorvastatin administered within 24 hours before CM exposure is effective in reducing the rate of CIAKI. This beneficial effect is observed only in patients at low to medium risk. http://circ.ahajournals.org/content/126/25/3008.long — Preceding unsigned comment added by Roomstop (talk • contribs) 00:02, 20 March 2013 (UTC)

Added a short synthesis section

...as a starting point for an eventual section that is a shorter, more complete, and pithier statement of general broad interest to non-chemists and chemists alike. (This is what I could do quickly, with available images and citations.) Cheers, see how this fits—many drug articles say how the drug is prepared, and here, it fit nicely in before the formulation section. Can't formulate something you haven't made. (Granted, better content is needed, and it can now more easily come.) Cheers. Le Prof Leprof 7272 (talk) 22:23, 14 June 2014 (UTC)

Request for POV/COI-type attention to lede/introduction, and Further reading

With all due respect due to Bruce Roth—truly, a great deal—the indicated parts of this article are overly representative of his contributions. I already toned down the lead, e.g., adding "and coworkers" and removing his alma mater, and called for a chemistry reference there. And to the chemistry references that I used, I added his coworkers names. Still, the Further reading is all about him, including a Chinese posting of an Amer Chem Soc award he received (?!). It reads like a cut and paste from a CV, or young student effort. Please, someone who works on these medical/drug articles, esp. with POV/COI/BLP experience here, scale this content back to an appropriate level, in these sections? Note, one of the Further reading articles now appears cited in the new synthesis section, and so I will start by deleting that from the further reading. Cheers, this is this community's item to take forward. Cheers. Le Prof Leprof 7272 (talk) 22:23, 14 June 2014 (UTC)

The same issues appear to be the case at the Roth BLP article. Help. Le Prof Leprof 7272 (talk) 23:36, 14 June 2014 (UTC)

Citations for Roth content in lede

In re: the citations regarding Bruce Roth in the lede: I am changing the patent to a secondary (review) source, and leaving in the "and coworkers" until secondary sourcing supports a sole synthesis/discovery role. Before giving the reasoning, please note, I added a section on atorvastatin synthesis. Though presently limited, it cites two Roth articles. Hence, he now receives more credit than he did in this article, when I began editing. Also, I am a former pharma chemist, univ chem faculty member, etc. Reasoning:

• The key articles appearing here on synthesis do not have Roth's name on them, alone.
• An article where one author presents/reviews his own work is not an appropriate secondary source to establish sole credit for discovery, because it lacks the independence WP requires. My saying (in primary or secondary literature or here) that I was the first to present on the now-popular cassette-type of approach to NP total synthesis that Sam Danishefsky is univerally known for, is just that: my saying it. Someone independent needs to say it, in a secondary source.
• Patents are primary sources. Patents and other such primary sources require WP:OR (original research) on the part of the WP editor—in establishing priority, interpreting information, etc. This is why secondary sources are the norm for medical and scientific writing here, correct?
• Without a further reliable secondary source indicating he was working on the compounds in isolation, with no assistance, no support structure, no staff—unless there are one or more single author publication in the primary literature establishing his being solely deserving of credit, reviewed and cited in independent secondary literature—the proper interpretation of an unbiased WP editor—I would argue to you—is to leave in the "and coworkers, where credit is given.

Bottom line: Because the citations in place do not establish that Roth solely deserves credit, and because the nature of pharma is that teams of people are usually involved and credited, I ask that you do not again remove "and coworkers" until it is very clearly supported by appropriate secondary sources (not patents, not news).

Placing the patent citation here, in case it is of use in finding an appropriate secondary source:

• REF START "Patent US4681893 - Trans-6-[2-(3- or 4-carboxamido-substituted pyrrol-1-yl)alkyl]-4 ... - Google Patents". REF CLOSE

Cheers. Le Prof Leprof 7272 (talk) 23:27, 14 June 2014 (UTC)

Hi LeProf-

By the strictest definition no one ever invented anything by themselves. But according the United States Manual of Patent Examination Procedure, the inventor is the one who “maintains intellectual domination of the work of making the invention down to the successful testing, selecting or rejecting….” and "The definition for inventorship can be simply stated: “The threshold question in determining inventorship is who conceived the invention. Unless a person contributes to the conception of the invention, he is not an inventor." and "Each joint inventor must generally contribute to the conception of the invention. A coinventor need not make a contribution to every claim of a patent. A contribution to one claim is enough"

Furthermore, the patent application must list all of the inventors. " Where an application names an incorrect inventorship, the applicant should submit a request to correct inventorship under 37 CFR 1.48. In the rare situation where it clear that the application does not name the correct inventorship and the applicant has not filed a request to correct inventorship under 37 CFR 1.48, Office personnel should reject the claims under 35 U.S.C. 101 and 35 U.S.C. 115. "

Thus the patent is a legal determination by the USPTO that Lipitor was indeed invented by Bruce Roth. Neither Bruce nor Thomas Edison, nor Samuel Morse, nor any other inventor in history worked in complete isolation and completely without the support of others. But we recognize those who "Maintained intellectual domination of the work making the invention". I'm sensitive to the fact that lots of people contributed to bringing Lipitor to the market. But they didn't invent it. Formerly 98 (talk) 00:09, 15 June 2014 (UTC)

@Formerly 98, as a pharma chemist I certainly agree with you. As a WP editor, I've stated what I understand to be the principles, policies and expectations, related to relying on patents (which require expertise and interpretation) vs upon derivative, secondary sources (which spoon feed us conclusions and most interpretation). Between us, honestly, I may trust you to make this call, but do I want every editor writing on chem or pharmacol doing this? (Pause, and think of all those you have come across here.) And if not, we are stuck—because the only way to differentiate is to allow for acknowledged expertise, and that is a verbotenes Thema.

So, I'll not revert, but I will bring it to an Admin's attention. Please, meanwhile, look for that secondary source, and pull the rug out from under me. I have no desire to fight truth (as this likely might be), but rules are there for a reason (and generally, not to create fights between knowledgeable and otherwise likely agreement-prone colleagues).

By the way, the other equitable solution to this would be to change it from "synthesis" to "discovered", whereupon my et al. becomes essential, unless you take the fully chemocentric tack that those doing assays, doing struct biol, etc. are not real discoverers (despite their being on the papers). How does one weigh review/monograph versus patent, when the rules of the WP site demand the one, and state we should not use the other, solely, as sources? As a chemist, even I can admit that patent policies at pharma are chem-centered vis-a-vis defining what involvement "contributes to the conception of the invention". (Having been in academia for a time now, I can tell you, academic mol bioscience types manage the exact opposite bias, as Lipinsky has talked about on the circuit.)

Bottom line, no chemist assays their own molecules, and nowadays few purify, determine structure, etc. What would our molecules be, without the rest of the team? If WP demands we (you and I) broaden from the patent perspective in assigning credit, it is absolutely fine by me. Cheers. Le Prof Leprof 7272 (talk) 01:46, 15 June 2014 (UTC)

@Formerly 98, hey, cheers. Holding off for the day at bring this to Admin. A last chance at persuasion. Have a look here WP:PATENTS, and here WP:ORGIND, and here WP:SPS. There it is, unless you see something that I do not. (And just saying, "well WP is wrong", as I often try, will not help.

So, have you found a secondary source that supports your OR on the patent—has someone else other than Roth-on-Roth written this up? It can be as simple as that.

Bottom line, I have no desire to pursue this, but cannot see the patent as being allowed to stand alone. Moreover, the Roth BLP article suffers from the same non-independent, non-encyclopedic thrust (compare further reading there and here, etc.). Help me help… Le Prof Leprof 7272 (talk) 08:49, 16 June 2014 (UTC)

I tend to see documents of this type as a special case. The requirement for secondary sources (which is not absoluate) is intended to prevent cherry picking among multiple studies that may not be reliable and or which may conflict with each other. But when citing a court ruling or official government agency decision, there are not multiple studies to cherry pick among. There is only one original patent for the drug, just like there is only one final verdict in a a court case.

If you really feel strongly about this, go ahead and change it back. I live in the states, where every scientific meeting I attend I meet someone who claims to the "THE inventor of Lipitor". This has happened dozens of times, and it gets a little old. I think credit is due to Roth and would like to see him get it, but it may be that I'm being too rigid about this.Formerly 98 (talk) 09:24, 16 June 2014 (UTC)

I think, in the interim, that the secondary source by Roth, and saying discovery by Roth et al, gives credit pretty clearly, and is a good placeholder for you, until you can find another secondary source, not by Roth, that says "Roth only". But we can also take this, amicably, to a Admin Noticeboard, and see what they say if you want. I am simply going by what I understand the guidelines to be, so as to set a good general exampe to folks far less experienced than we are. Only down side of taking this to a Noticeboard, is that you may not find scientific expertise that appreciates your perspective (as much as I do), only WP expertise. So, will change to Roth review, but (i) keep an eye out for a replacement ref. that allows us to drop the et al, and let me know if you want me to take this to a Noticeboard for another opinion. Cheers. Le Prof Leprof 7272 (talk)

I have read the above and I agree with Formerly. For documenting inventorship, a patent is a very relevant document. I therefore have restored it. Boghog (talk) 13:31, 23 July 2014 (UTC)

Price information

The consensus of the RfC was not to scrub all pricing information from Wikipedia. So moved it to the body of the text. Doc James (talk · contribs · email) 19:12, 31 March 2020 (UTC)

How about removing all mention of pricing from the lede per the RfC and the content policies cited there? --Hipal/Ronz (talk) 20:17, 1 April 2020 (UTC)

Any objections to my removing it from the lede per RfC and policies? --Hipal/Ronz (talk) 16:07, 2 April 2020 (UTC)

I've gone ahead and remove the pricing and generic availability from the lede, leaving the content in the article body untouched. I'm happy to explain further, though I think it's pretty clear from the recent RfC: Wikipedia:Manual of Style/Medicine-related articles/RFC on pharmaceutical drug prices --Hipal/Ronz (talk) 16:01, 4 April 2020 (UTC)

Of course plenty of objection and we have a RfC here Talk:Simvastatin#Clarification_of_RfC were support is overwhelming. Doc James (talk · contribs · email) 17:11, 4 April 2020 (UTC)