Troglitazone: Difference between revisions
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'''Troglitazone''' (Rezulin, Resulin or Romozin) is an [[anti-diabetic]] and [[antiinflammatory]] drug, and a member of the [[medication|drug]] class of the [[thiazolidinedione]]s. It was developed by [[Daiichi Sankyo Co.]](Japan). It was introduced and manufactured by [[Parke-Davis]] in the late 1990s but turned out to be associated with an idiosyncratic reaction leading to drug-induced [[hepatitis]]. |
'''Troglitazone''' (Rezulin, Resulin or Romozin) is an [[anti-diabetic]] and [[antiinflammatory]] drug, and a member of the [[medication|drug]] class of the [[thiazolidinedione]]s. It was developed by [[Daiichi Sankyo Co.]](Japan). It was introduced and manufactured by [[Parke-Davis]] in the late 1990s, but turned out to be associated with an idiosyncratic reaction leading to drug-induced [[hepatitis]]. One FDA medical officer evaluating troglitazone, John Gueriguian, did not recommend its approval due to potential high liver toxicity,<ref>[http://www.wired.com/medtech/drugs/multimedia/2008/10/gallery_retired_drugs?slide=6&slideView=6 Retired Drugs: Failed Blockbusters, Homicidal Tampering, Fatal Oversights], wired.com</ref> but a full panel of experts approved it in January 1997.<ref>{{cite journal | doi = 10.1007/s00125-006-0245-0}}</ref> Subsequently, once the prevalence of adverse liver effects became known, troglitazone was withdrawn from the [[United Kingdom]] market in December 1997, from the [[USA]] market in 2000, and from the [[Japan]] market soon afterwards. |
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It was withdrawn from the [[United Kingdom]] market (sold by [[Glaxo]]) in December 1997, from the [[USA]] market on 21 March 2000, and from the [[Japan]] markets soon afterwards. |
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==Mode of action== |
==Mode of action== |
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Troglitazone, like the other [[thiazolidinedione]]s ([[pioglitazone]] and [[rosiglitazone]]), works by activating [[peroxisome proliferator-activated receptor|PPAR]]s (peroxisome proliferator-activated receptors). |
Troglitazone, like the other [[thiazolidinedione]]s ([[pioglitazone]] and [[rosiglitazone]]), works by activating [[peroxisome proliferator-activated receptor|PPAR]]s (peroxisome proliferator-activated receptors). |
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Troglitazone is a ligand to both PPARα and - more strongly - PPARγ. Troglitazone also contains an α-tocopheroyl moiety, potentially giving it [[vitamin E]]-like activity in addition to its PPAR activation. It has been shown (Aljada ''et al.'') to reduce [[inflammation]]: troglitazone use was associated with a decrease of |
Troglitazone is a ligand to both PPARα and - more strongly - PPARγ. Troglitazone also contains an α-tocopheroyl moiety, potentially giving it [[vitamin E]]-like activity in addition to its PPAR activation. It has been shown (Aljada ''et al.'') to reduce [[inflammation]]: troglitazone use was associated with a decrease of [[NF-κB|nuclear factor kappa-B]] (NF-κB) and a concomitant increase in its inhibitor (IκB). NFκB is an important cellular transcription regulator for the immune response. |
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==References== |
==References== |
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Revision as of 18:24, 29 March 2010
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| Elimination half-life | 16-34 hours |
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| Chemical and physical data | |
| Formula | C24H27NO5S |
| Molar mass | 441.541 g/mol g·mol−1 |
Troglitazone (Rezulin, Resulin or Romozin) is an anti-diabetic and antiinflammatory drug, and a member of the drug class of the thiazolidinediones. It was developed by Daiichi Sankyo Co.(Japan). It was introduced and manufactured by Parke-Davis in the late 1990s, but turned out to be associated with an idiosyncratic reaction leading to drug-induced hepatitis. One FDA medical officer evaluating troglitazone, John Gueriguian, did not recommend its approval due to potential high liver toxicity,[1] but a full panel of experts approved it in January 1997.[2] Subsequently, once the prevalence of adverse liver effects became known, troglitazone was withdrawn from the United Kingdom market in December 1997, from the USA market in 2000, and from the Japan market soon afterwards.
Mode of action
Troglitazone, like the other thiazolidinediones (pioglitazone and rosiglitazone), works by activating PPARs (peroxisome proliferator-activated receptors).
Troglitazone is a ligand to both PPARα and - more strongly - PPARγ. Troglitazone also contains an α-tocopheroyl moiety, potentially giving it vitamin E-like activity in addition to its PPAR activation. It has been shown (Aljada et al.) to reduce inflammation: troglitazone use was associated with a decrease of nuclear factor kappa-B (NF-κB) and a concomitant increase in its inhibitor (IκB). NFκB is an important cellular transcription regulator for the immune response.
References
- ^ Retired Drugs: Failed Blockbusters, Homicidal Tampering, Fatal Oversights, wired.com
- ^ . doi:10.1007/s00125-006-0245-0.
{{cite journal}}: Cite journal requires|journal=(help); Missing or empty|title=(help)
- Aljada A, Garg R, Ghanim H; et al. (2001). "Nuclear factor-kappaB suppressive and inhibitor-kappaB stimulatory effects of troglitazone in obese patients with type 2 diabetes: evidence of an antiinflammatory action?". J. Clin. Endocrinol. Metab. 86 (7): 3250–6. doi:10.1210/jc.86.7.3250. PMID 11443197.
{{cite journal}}: Explicit use of et al. in:|author=(help)CS1 maint: multiple names: authors list (link)
External links
- Diabetes Monitor article on troglitazone
- RxList article on troglitazone