Lornoxicam dose relatedly reduces the total number of c-Fos-LI neurons with the strongest effect corresponding to the 75% reduction for the highest dose of 9 mg/kg, and the 45% reduction for the low dose of 0.3 mg/kg. Lornoxicam (0.1, 0.3 mg/kg, 1 mg/kg, 3 mg/kg and 9 mg/kg, i.v.) significantly reduces the number of c-Fos-LI neurons in both superficial (24%, 33%, 53%, 54%, and 63% reduction, respectively) and deep (28%, 48%, 62%, 69% and 79% reduction, respectively) laminae of the dorsal horn of the spinal cord. Lornoxicam reduces hyperalgesia with an effective dose that provides 50% inhibition (ED50) of 0.083 mg/kg, 3.9 mg/kg and 4.3 mg/kg respectively in a chronic rat model of arthritis. Lornoxicam significantly reduces the PGE2 level in paw exudate and the cerebrospinal fluid in rats. Lornoxicam 0.16 mg/kg, celecoxib 4 mg/kg and loxoprofen 2.4 mg/kg significantly reduces hyperalgesia to a similar extent in acute oedematous rats.

Absorption, Distribution and Excretion
Lornoxicam is absorbed rapidly and almost completely from the GI tract (90-100%).

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Metabolism / Metabolites
Lornoxicam is metabolized completely by cyp 2C9 with the principal metabolite being 5'-hydroxy-lornoxicam and only negligible amounts of intact lornoxicam are excreted unchanged in the urine. Approximately 2/3 of the drug is eliminated via the liver and 1/3 via the kidneys in the active form.
Lornoxicam has known human metabolites that include 5'-Hydroxylornoxicam.

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Biological Half-Life
3-5 hours

Protein Binding
Lornoxicam is 99% bound to plasma proteins (almost exlusively to serum albumin).

Drugs.1996 Apr;51(4):639-57;Inflammopharmacology.1997;5(4):331-41.

Lornoxicam is a thienothiazine-derived monocarboxylic acid amide obtained by formal condensation of the carboxy group of 6-chloro-4-hydroxy-2-methylthieno[2,3-e][1,2]thiazine-3-carboxylic acid 1,1-dioxide with the amino group of 2-aminopyridine. Used for the treatment of pain, primarily resulting from inflammatory diseases of the joints, osteoarthritis, surgery, sciatica and other inflammations. It has a role as a non-steroidal anti-inflammatory drug, a non-narcotic analgesic and an antipyretic. It is a thienothiazine, a member of pyridines, a monocarboxylic acid amide, an organochlorine compound and a heteroaryl hydroxy compound.
Lornoxicam (chlortenoxicam) is a new nonsteroidal anti-inflammatory drug (NSAID) of the oxicam class with analgesic, anti-inflammatory and antipyretic properties. Lornoxicam differs from other oxicam compounds in its potent inhibition of prostaglandin biosynthesis, a property that explains the particularly pronounced efficacy of the drug. Lornoxicam is approved for use in Japan.
Lornoxicam is an orally bioavailable oxicam and non-steroidal anti-inflammatory drug (NSAID), with analgesic, anti-pyretic, anti-thrombotic and anti-inflammatory activities. Upon oral administration, lornoxicam binds to and inhibits the activity of the cyclooxygenase enzymes (COX) type 1 (COX-1) and type 2 (COX-2). This blocks COX-mediated signaling pathways, which leads to reduced prostaglandin and thromboxane production and decreased pain, fever and inflammation.

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Drug Indication
For the treatment of acute mild to moderate pain, as well as pain and inflammation of the joints caused by certain types of rheumatic diseases.

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Mechanism of Action
Like other NSAIDS, lornoxicam's anti-inflammatory and analgesic activity is related to its inhibitory action on prostaglandin and thromboxane synthesis through the inhibition of both COX-1 and COX-2. This leads to the reduction of inflammation, pain, fever, and swelling, which are mediated by prostaglandins. However, the exact mechanism of lornoxicam, like that of the other NSAIDs, has not been fully determined.

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Pharmacodynamics
Lornoxicam is a non-steroidal anti-inflammatory drug (NSAID) that belongs to the oxicam class. As with other NSAIDS, lornoxicam is a potent inhibitor of the cyclooxgenase enzymes, which are responsible for catalyzing the formation of prostaglandins (act as messenger molecules in the process of inflammation) and thromboxane from arachidonic acid. Unlike some NSAIDS, lornoxicam's inhibition of cyclooxygenase does not lead to an increase in leukotriene formation, meaning that arachidonic acid is not moved to the 5-lipoxygenase cascade, resulting in the minimization of the risk of adverse events.

C13H10CLN3O4S2

371.82

370.98

70374-39-9

Lornoxicam-d4;1216527-48-8

54690031

Light yellow to yellow solid powder

1.7±0.1 g/cm3

225-230°C (dec.)

1.741

2.18

2

7

2

23

634

0

WLHQHAUOOXYABV-UHFFFAOYSA-N

InChI=1S/C13H10ClN3O4S2/c1-17-10(13(19)16-9-4-2-3-5-15-9)11(18)12-7(23(17,20)21)6-8(14)22-12/h2-6,18H,1H3,(H,15,16,19)

6-chloro-4-hydroxy-2-methyl-1,1-dioxo-N-pyridin-2-ylthieno[2,3-e]thiazine-3-carboxamide

2934.99.9001

Powder      -20°C    3 years

                     4°C     2 years

In solvent   -80°C    6 months

                  -20°C    1 month

Room temperature (This product is stable at ambient temperature for a few days during ordinary shipping and time spent in Customs)