Salicylsalicylic acid

258.23

258.23

209-027-4

V9MO595C9I

755823|49171

DTXSID1023572

C62636

N - Nervous system

2918990090

83.8

3

white to tan Crystalline Powder

1.4±0.1 g/cm3

147 °C

482.9°C at 760 mmHg

188.0±16.7 °C

1.646

HYDROLYSIS;DMSO: ≥15mg/mL

room temp

151.3 Ų [M+H]+ [CCS Type: TW, Method: calibrated with polyalanine and drug standards]

Ⅲ

UN 3077 9 / PGIII

3

36/37/38-50-22

37/39-26-61

DH2080000

Xi,N,Xn

Stable at room temperature in closed containers under normal storage and handling conditions.

P301 + P312 + P330

H302-H400

|Warning|H302 (86.96%): Harmful if swallowed [Warning Acute toxicity, oral]|P261, P264, P270, P271, P273, P280, P301+P312, P302+P352, P304+P340, P305+P351+P338, P312, P321, P330, P332+P313, P337+P313, P362, P391, P403+P233, P405, and P501|Aggregated GHS information provided by 46 companies from 5 notifications to the ECHA C&L Inventory. Each notification may be associated with multiple companies.

Death has followed ingestion of 10 to 30 g of salicylates in adults, but much larger amounts have been ingested without fatal outcome.

Prospective studies show that a proportion of patients taking salsalate experience at least transient serum aminotransferase elevations particularly when it is given in higher doses. These abnormalities may resolve even with drug continuation or after dose reduction. Marked aminotransferase elevations (>10 fold elevated) occur rarely except with use of higher doses (4 g daily or more) in a manner similar to aspirin. Clinically apparent liver injury with jaundice from salsalate has not been reported and must be very rare. Salsalate is probably capable of inducing Reye syndrome in a susceptible child or adolescent and, like aspirin, should be avoided in those age groups.

Salicylate: 90-95% bound at plasma salicylate concentrations <100 mcg/mL; 70-85% bound at concentrations of 100-400 mcg/mL; 25-60% bound at concentrations >400 mcg/mL.

For relief of the signs and symptoms of rheumatoid arthritis, osteoarthritis and related rheumatic disorders.

Salsalate is a nonacetylated dimer of salicylic acid that is used in the treatment of chronic arthritis as an analgesic and antipyretic. Salsalate can cause moderate serum aminotransferase elevations when given in high doses in a manner similar to aspirin.

Antiinflammatory Agents

Salsalate is a nonsteroidal anti-inflammatory agent for oral administration. Salsalate's mode of action as an anti-inflammatory and antirheumatic agent may be due to inhibition of synthesis and release of prostaglandins. The usefulness of salicylic acid, the active in vivo product of salsalate, in the treatment of arthritic disorders has been established. In contrast to aspirin, salsalate causes no greater fecal gastrointestinal blood loss than placebo.

Anti-inflammatory agents that are non-steroidal in nature. In addition to anti-inflammatory actions, they have analgesic, antipyretic, and platelet-inhibitory actions.They act by blocking the synthesis of prostaglandins by inhibiting cyclooxygenase, which converts arachidonic acid to cyclic endoperoxides, precursors of prostaglandins. Inhibition of prostaglandin synthesis accounts for their analgesic, antipyretic, and platelet-inhibitory actions; other mechanisms may contribute to their anti-inflammatory effects. (See all compounds classified as Anti-Inflammatory Agents, Non-Steroidal.)

Salsalate is insoluble in acid gastric fluids (< 0.1 mg/ml at pH 1.0), but readily soluble in the small intestine where it is partially hydrolyzed to two molecules of salicylic acid. A significant portion of the parent compound is absorbed unchanged. The amount of salicylic acid available from salsalate is about 15% less than from aspirin, when the two drugs are administered on a salicylic acid molar equivalent basis (3.6 g salsalate/5 g aspirin). Food slows the absorption of all salicylates including salsalate.

Salsalate is readily soluble in the small intestine where it is partially hydrolyzed to two molecules of salicylic acid. A significant portion of the parent compound is absorbed unchanged and undergoes rapid esterase hydrolysis in the body.

The parent compound has an elimination half-life of about 1 hour. Salicylic acid (the active metabolite) biotransformation is saturated at anti-inflammatory doses of salsalate. Such capacity limited biotransformation results in an increase in the half-life of salicylic acid from 3.5 to 16 or more hours.

The mode of anti-inflammatory action of salsalate and other nonsteroidal anti-inflammatory drugs is not fully defined, but appears to be primarily associated with inhibition of prostaglandin synthesis. This inhibition of prostaglandin synthesis is done through the inactivation of cyclooxygenase-1 (COX-1) and COX-2, which are reponsible for catalyzing the formation of prostaglandins in the arachidonic acid pathway. Although salicylic acid (the primary metabolite of salsalate) is a weak inhibitor of prostaglandin synthesis in vitro, salsalate appears to selectively inhibit prostaglandin synthesis in vivo, providing anti-inflammatory activity equivalent to aspirin and indomethacin. Unlike aspirin, salsalate does not inhibit platelet aggregation.

Arcylate

Benzoic acid, 2-hydroxy-, 2-carboxyphenyl ester: INACTIVE