ジクロフェナクナトリウム

Breast Feeding; Lactation; Milk, Human; Analgesic Agents; Anti-inflammatory Agents, Nonsteroidal

FDA approved drugs -> Active ingredient

FDA approved drugs -> Active ingredient

Danger

H301 (96.7%): Toxic if swallowed [Danger Acute toxicity, oral]

P203, P260, P261, P264, P264+P265, P270, P271, P273, P280, P301+P316, P302+P352, P304+P340, P305+P351+P338, P316, P318, P319, P321, P330, P332+P317, P337+P317, P362+P364, P391, P403+P233, P405, and P501 (click each P-code to see the statement)

Aggregated GHS information provided per 243 reports by companies from 43 notifications to the ECHA C&L Inventory. Each notification may be associated with multiple companies.

Status: Active Update: 27-05-2019 https://echa.europa.eu/registration-dossier/-/registered-dossier/13423

Diclofenac sodium: Does not have an individual approval but may be used under an appropriate group standard

The antiinflammatory effects of diclofenac are believed to be due to inhibition of both leukocyte migration and the enzyme cylooxygenase (COX-1 and COX-2), leading to the peripheral inhibition of prostaglandin synthesis. As prostaglandins sensitize pain receptors, inhibition of their synthesis is responsible for the analgesic effects of diclofenac. Antipyretic effects may be due to action on the hypothalamus, resulting in peripheral dilation, increased cutaneous blood flow, and subsequent heat dissipation.

Hepatic. Route of Elimination: Diclofenac is eliminated through metabolism and subsequent urinary and biliary excretion of the glucuronide and the sulfate conjugates of the metabolites. Little or no free unchanged diclofenac is excreted in the urine. Approximately 65% of the dose is excreted in the urine and approximately 35% in the bile as conjugates of unchanged diclofenac plus metabolites. Half Life: 2 hours

DICLOFENAC SODIUM

Cyclooxygenase Inhibitors [MoA]; Nonsteroidal Anti-inflammatory Drug [EPC]; Anti-Inflammatory Agents, Non-Steroidal [CS]; Decreased Prostaglandin Production [PE]

DICLOFENAC SODIUM 1%

Cyclooxygenase Inhibitors [MoA]; Anti-Inflammatory Agents, Non-Steroidal [CS]; Decreased Prostaglandin Production [PE]; Nonsteroidal Anti-inflammatory Drug [EPC]

DICLOFENAC SODIUM D/R

Cyclooxygenase Inhibitors [MoA]; Nonsteroidal Anti-inflammatory Drug [EPC]; Decreased Prostaglandin Production [PE]; Anti-Inflammatory Agents, Non-Steroidal [CS]

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.

Compounds or agents that combine with cyclooxygenase (PROSTAGLANDIN-ENDOPEROXIDE SYNTHASES) and thereby prevent its substrate-enzyme combination with arachidonic acid and the formation of eicosanoids, prostaglandins, and thromboxanes.