Talk:Moxifloxacin

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Information added

I add an information for patients section because the article is too technical otherwise. KlausFr

I've removed this section because all the information in it is already noted elsewhere in the article. ~ Amalas rawr =^_^= 21:03, 15 March 2007 (UTC)[reply]

Update

On 2008/FEB/13 or so, Bayer released a warning that severity of side effects had been underestimated. Dysmorodrepanis (talk) 19:43, 15 February 2008 (UTC)[reply]

As someone that was fairly healthy prior to taking this drug, I can tell you that you should NOT take this drug unless it is a life/death situation. This Antibiotic / body killer is VERY VERY aggressive and should be noted as such in this wiki as best as possible. This is a last line of defense antibiotic that is heavily over prescribed. —Preceding unsigned comment added by 71.61.125.253 (talk) 03:33, 16 December 2008 (UTC)[reply]

Comments

The first line of this entry says Moxifloxacin is a third-gen but the chart below shows it as a fourth-gen..which is correct? --writing a paper / thanks, jag —Preceding unsigned comment added by 71.145.130.131 (talk) 20:21, 7 October 2009 (UTC)[reply]

Actually both. This type of confusion is quite common with this class. Depending on the author/publication it could be considered either one. Both are correct as it is listed as both within the literature depending on who wrote the article and when the article was written. For your paper I would simply make note of this within a footnote stating that it is listed by some researchers as a third generation, and by others as a fourth.Davidtfull (talk) 23:44, 7 October 2009 (UTC)[reply]

Moxifloxacin is often referred to as a chemotherapeutic drug because its mode of action has so far not been noted in any naturally occurring or semi-synthetic antibiotic.

Is this correct? Chemotherapeutic means a drug which has a high toxicity for select types of cells, in this case bacterial cells. If my moderate knowledge on antibiotics is correct most other antibiotic classes inhibit replication or growth of bacteria whereas quinolones are directly toxic and directly kill bacteria hence why they are chemotherapeutic.--Literaturegeek | T@1k? 01:50, 10 April 2009 (UTC)[reply]

No, I do not believ that statement to be technically correct. In its broadest definition, an antibiotic is any drug that interferes with the growth and reproduction of bacteria. The term chemotherapuetic refers to the treatment of disease using chemical agents or drugs that are selectively toxic to the causative agent of the disease, such as a virus, bacterium, or other microorganism. Where as antibacterials are anything that destroys bacteria or suppresses their growth or their ability to reproduce.
Sulfa drugs for instance are analogs of PABA; they compete with PABA and, when chosen, block the synthesis of folic acid. Both bacteria and their human hosts require folic acid for nucleic acid synthesis (it is converted into purines and thymidine) as well as protein synthesis (precursor of the amino acids methionine and glycine). Hence sulfa drugs work by blocking the synthesis of folic acid required by the bacteria, thereby erradicating it.
The beta-lactams all work by interfering with the synthesis of the bacterial cell wall. The beta-lactam antibiotics bind to and inhibit enzymes needed for the synthesis of the peptidoglycan wall. While they have little effect on resting bacteria, they are lethal to dividing bacteria as defective walls cannot protect the organism.
As far as the semi-synthetic derivatives go, Aminoglycosides bind to the 30S subunit of the bacterial ribosome and interfere with the formation of the initiation complex thereby cause misreading of the mRNA. Tetracyclines work in pretty much the same manner. Tetracyclines also bind to the 30S subunit of the bacterial ribosome. They prevent the transfer of activated amino acids to the ribosome so protein synthesis is halted. Macrolides, Lincosamides, Streptogramins also follow the same general prinicple as all these antibiotics bind to the 23S rRNA molecule in the large (50S) subunit of the bacterial ribosome where they block the elongation of the growing peptide chain.
Where as the fluoroquinolones are believed to block the action of two bacterial topoisomerases — enzymes that relieve the coils that form in DNA when the helix is being opened in preparation for replication or transcription or repair. Something we do NOT see with ANY other drug used to treat bacterial infections. As such the following statement is an opinion, not a fact:
Moxifloxacin is often referred to as a chemotherapeutic drug because its mode of action has so far not been noted in any naturally occurring or semi-synthetic antibiotic.
Moxifloxacin is referred to as a chemotherapuetic drug because moxifloxacin IS, by definition, a chemotherapuetic drug. Semi-synthetic antibiotics, as noted above, are NOT by definition to be considered chemotherapuetic agents and thus in the same category as the fluoroquinolones. The fluoroquinolones interfere with the replication process on a DNA level, hence selectively toxic to the causative agent, rather than interfering with one or more of the key elements needed for the actual synthesis process of the bacterium. As such I believe this statement should be removed from the article and subsituted with a factual one instead. But the article still needs a lot of work, so I intended to just let this slide until I finish with the rewrite. I plan on using the same definition I used on the levaquin and cipro articles when the time comes. Davidtfull (talk) 04:33, 10 April 2009 (UTC)[reply]

trade names

It had been stated that: there is a long-standing saying in Wikipedia (it may even be codified somewhere) that "redirects are cheap". Therefore it had been suggested that: redirects for trade names are a more appropriate solution than in-article "laundry" lists, because 1) they avoid clutter in the article body, 2) they prevent issues such as an ever-growing list that may be "expanded" with inaccurate information and 3) they make it much easier for someone looking for a particular generic formulation of the drug to get to the actual article. Since this suggestion is both practical and logical I have removed the list of trade names and used redirects instead. As such someone searching Wikipedia using a brand name would simply be taken directly to the levaquin article.

I would now ask that editors not expand the trade name list, but create redirects instead. Those not familiar with this process may find the following article helpful:

http://en.wikipedia.org/wiki/Wikipedia:Redirect

Davidtfull (talk) 01:39, 19 May 2009 (UTC)[reply]

Article currently being reviewed and revised as needed

Please do not engage in deletions or additions while the article is being updated and revised as needed by the primary editors. It would be appreciated if potential editors would post all such concerns on this talk page for discussion to avoid unneccasary confusion during this process. Once these major revisions are completed this notice will be removed and such editors are invited to improve the article as they see fit. Davidtfull (talk) 08:34, 21 July 2009 (UTC)[reply]

It appears that the major revisions have been completed. As such editors are invited to improve the article as they see fit.Davidtfull (talk) 01:43, 29 July 2009 (UTC)[reply]

Just as a side note: I appreciate your contributions, however, no editors own an article, and there are really no primary editors. Any editor can edit any article at any time (assuming its not locked in some manner). The easiest way to make improvements to an article that you don't want others to work on while you are doing is to use a subpage in userspace :-) Fuzbaby (talk) 22:51, 29 July 2009 (UTC)[reply]

Appreciate the suggestion as well, but I had pretty much given up doing any more work on these articles. The major revisions and editing was being done by Literature Geek, not I. I was just asking the deletionists to cut him some slack for a few days is all. Not that I really expected anybody to listen but I saw no harm in asking.Davidtfull (talk) 03:39, 30 July 2009 (UTC)[reply]

Revisions of the regulator section

This discussion was originally posted on the levaquin talk page with notice given to all editors involved regarding this proposed change as it involved all the fluoroquinolone drug articles. Similar edits are planned for those other articles as well. Please refer to that discussion regarding these recent edits involving the regulatory section if you have any questions or concerns regarding them.Davidtfull (talk) 08:24, 25 July 2009 (UTC)[reply]

Remaining issues

I have been doing a bit of a clean up of the article and I have almost finished if it weren't for two sections with continuing problems with them. I have some remaining issues which I am raising for discussion. Problem one concerns this section Moxifloxacin#Social_and_economic_impact, see also this diff. Two refs are to a blog, blogs are almost never considered a reliable source, these refs will need to be replaced or else the cited text and blog refs deleted. Another ref is a dead link and needs to be replaced or else deleted along with cited text. Problem two concerns this section Moxifloxacin#Risk.2Fbenefit_ratio, see also this diff. If you look at the diff carefully you will see that I have added 6 hidden comments requesting additional info such as urls and titles for the citations to track them down. There is also a hidden comment which you can see in the edit diff regarding a citation which replaced a 1986 citation without the cited text being updated to reflect the new source.--Literaturegeek | T@1k? 20:55, 13 August 2009 (UTC)[reply]

These issues will need to be resolved or else we will have to think about pruning out/deleting these problematic statements and citations.--Literaturegeek | T@1k? 23:16, 13 August 2009 (UTC)[reply]

Indeed. The article remains extremely unbalanced. Fvasconcellos (t·c) 01:33, 19 August 2009 (UTC)[reply]

I've expanded the references as requested providing urls to the original text cited to and fixed the references that had been screwed with and deleted by others. As such I believe this resolves the issues that had been raised here. But it appears that Fvasconcellos is suggesting we delete this whole section so this raises yet another set of unresolved issues that needs to be dealt with before moving on.Davidtfull (talk) 23:43, 19 August 2009 (UTC)[reply]

Thank you for providing the URLs. I had to delete some content as the refs were specifically on levofloxacin. I did however, leave a see also link for people to click on if they want further info on the levofloxacin article. I also moved some content to the maiin quinolone article, again leaving a see also link for readers to click if they are interested in reading further. I have also made most of the citations inline citations. I think that the article is much better. More work can be done to it of course but I think that now that the article is reasonable it is better for me and us to move onto other articles and tidy them up, for example ciprofloxacin is in need of a make over. I intend to make that my next project.--Literaturegeek | T@1k? 08:54, 29 August 2009 (UTC)[reply]

Mechanism of action

I removed much of the discussion of DNA damage, cytotoxicity, and related speculation regarding side effects of moxifloxacin from this section. I agree that the topic is an important one, but the problems with the section seemed to be irretrievable.

1) None of the references described results obtained with moxifloxacin, and indeed most were studies of structural analogs of the fluoroquinolones that were never licensed for use in humans. There is no way of knowing whether the results obtained with these analogs are applicable to the compound which is the subject of the article.

2) Many of the references, which claimed to support DNA damage, in fact document related but distinct phenomena, such as inhibition of the synthesis of DNA precursors.

3) Other cited references refer simply to unsourced statements made in introductory paragraphs of papers published in obscure journals such as the Brazilian Journal of Chemistry. As a PhD chemist with 20 years of industry experience, I have never encountered this journal until today.

4) All cited references were in vitro studies, using methods that have been shown in some cases to be highly dependent on variables such as medium ionic strength. Thus their applicability to the in vivo situation is unknown.

Overall, one must ask, if the possibility of DNA damage by the moxifloxacin is mainstream medical thought, why does one need to go to studies involving non-marketed structural analogs, many of which were published in obscure journals, to find supporting references?

I deleted this material as speculative and placing excess weight on studies that do not involve the subject compound. — Preceding unsigned comment added by Alfred Bertheim (talkcontribs) 19:25, 13 January 2013 (UTC)[reply]

Mechanism of action

I removed much of the discussion of DNA damage, cytotoxicity, and related speculation regarding side effects of moxifloxacin from this section. I agree that the topic is an important one, but the problems with the section seemed to be irretrievable.

1) None of the references described results obtained with moxifloxacin, and indeed most were studies of structural analogs of the fluoroquinolones that were never licensed for use in humans. There is no way of knowing whether the results obtained with these analogs are applicable to the compound which is the subject of the article.

2) Many of the references, which claimed to support DNA damage, in fact document related but distinct phenomena, such as inhibition of the synthesis of DNA precursors.

3) Other cited references refer simply to unsourced statements made in introductory paragraphs of papers published in obscure journals such as the Brazilian Journal of Chemistry. As a PhD chemist with 20 years of industry experience, I have never encountered this journal until today.

4) All cited references were in vitro studies, using methods that have been shown in some cases to be highly dependent on variables such as medium ionic strength. Thus their applicability to the in vivo situation is unknown.

Overall, one must ask, if the possibility of DNA damage by the moxifloxacin is mainstream medical thought, why does one need to go to studies involving non-marketed structural analogs, many of which were published in obscure journals, to find supporting references?

I deleted this material as speculative and placing excess weight on studies that do not involve the subject compound. — Preceding unsigned comment added by Alfred Bertheim (talkcontribs) 19:27, 13 January 2013 (UTC)[reply]

Useful reference

Peterson, U. (2006). "Quinolone Antibiotics: The Development of Moxifloxacin". In IUPAC; Fischer, J.; Ganellin, C. R. (eds.). Analogue-based Drug Discovery. John Wiley & Sons. pp. 338–342. ISBN 9783527607495.

This book has an entire chapter on moxifloxacin, much of it available on Google Books. May be useful for someone.  :) EdChem (talk) 12:02, 28 December 2015 (UTC)[reply]

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