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Lornoxicam: Wikis


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Systematic (IUPAC) name
(3E)-6-chloro-3-[hydroxy(pyridin-2-ylamino)methylene]-2-methyl-2,3-dihydro-4 H-thieno[2,3-e][1,2]thiazin-4-one 1,1-dioxide
CAS number  ?
ATC code M01AC05
PubChem 5282204
Chemical data
Formula C 13H10ClN3O4S2  
Mol. mass 371.8192 g/mol
Pharmacokinetic data
Bioavailability  ?
Metabolism  ?
Half life  ?
Excretion  ?
Therapeutic considerations
Pregnancy cat.  ?
Legal status
Routes  ?

Lornoxicam (chlortenoxicam) is a non-steroidal anti-inflammatory drug (NSAID) of the oxicam class with analgesic, anti-inflammatory and antipyretic properties. It is available in oral and parenteral formulations.



Mode of action

Like other NSAIDs, lornoxicam inhibits prostaglandin biosynthesis by blocking the enzyme cyclooxygenase.

Lornoxicam inhibits both isoforms in the same concentration range, that is, COX-1 inhibition : COX-2 inhibition = 1. It readily penetrates into the synovial fluid. Synovial fluid : plasma AUC ratio is 0.5 after administration of 4 mg twice daily.



Lornoxicam is absorbed rapidly and almost completely from the gastro-intestinal tract. Maximum plasma concentrations are achieved after approximately 1 to 2 hours.


The absolute bioavailability of Lornoxicam is 90-100%. No first-pass effect was observed.


Lornoxicam is found in the plasma in unchanged form and as its hydroxylated metabolite. The hydroxylated metabolite exhibits no pharmacological activity. CYP2C9 has been shown to be the primary enzyme responsible for the biotransformation of the lornoxicam to its major metabolite, 5’-hydroxylor noxicam. Recently, it was reported that lornoxicam 5’-hydroxylation by the variant CYP2C9*3 and CYP2C9*13 was markedly reduced compared with wild type, both in vitro and in vivo.


Approximately 2/3 is eliminated via the liver and 1/3 via the kidneys as inactive substance.

Three of the most commonly employed substrate probes for determining CYP2C9 activity in crude human tissue fractions are (S)-warfarin (7-hydroxylation), tolbutamide (methylhydroxylation), and diclofenac (4-hydroxylation). And the best in vivo probes for CYP2C9 activity are tolbutamide and flurbiprofen. Turnover of (S)-warfarin and tolbutamide by CYP2C9 is extremely slow. Conversely, diclofenac has the advantage that CYP2C9 catalyzes its metabolism with a high turnover number, but is not a useful in vivo probe for the CYP2C9 enzyme.

We suggest lornoxicam as a good Probe for CYP2C9, both In Vitro and In Vivo. First, turnover of lornoxicam by CYP2C9 is much faster than (S)-warfarin and tolbutamide. So it is beneficial in allowing for facile, economical HPLC-UV assays to be employed for routine screening in vitro. Second, the lornoxicam poor metabolizer we found who is heterozygous for the CYP2C9*13 together with the CYP2C9*3, i.e. with the invalidated CYP2C9, has the lornoxicam half-life of about 105 h, indicating the specific biotransformation of the NSAID by CYP2C9.[1] [2]

Drug Interactions


8 mg to 16 mg per day in 2 to 3 doses. The total daily dose should not exceed 16 mg.

Brand names

  • Lorna tablets
  • Lornox
  • Lorsaid injection
  • Nyox tablets
  • Xefo Rapid tablets
  • Xefocam tablets and injection


  1. ^ Zhang Yifan, Zhong Dafang*, Si Dayong, Guo Yingjie, Chen Xiaoyan, Zhou Hui. Lornoxicam pharmacokinetics in relation to cytochrome P450 2C9 genotype. The British Journal of Clinical Pharmacology. 2005 Jan;59(1):14-7.
  2. ^ Guo Yingjie, Zhang Yifan, Wang Ying, Chen Xiaoyan, Si Dayong, Zhong Dafang, Fawcett JP, Zhou Hui*. Role of CYP2C9 and its variants (CYP2C9*3 and CYP2C9*13) in the metabolism of lornoxicam in human. Drug Metab Dispos. 2005 Jun;33(6):749-53.

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