Morniflumate

395.38

395.38

R133MWH7X1

DTXSID6057798

M - Musculo-skeletal system

2934999090

63.69000

4.79

1.3±0.1 g/cm3

75-77°C

478.2±45.0 °C at 760 mmHg

243.0±28.7 °C

1.555

soluble in DMSO

|Warning|H302 (100%): Harmful if swallowed [Warning Acute toxicity, oral]|P264, P270, P280, P301+P312, P302+P352, P321, P330, P332+P313, P362, and P501|The GHS information provided by 1 company from 1 notification to the ECHA C&L Inventory.

As with other anti-inflammatory medications, adverse effects may include: agranulocytosis, bleeding, hepatotoxicity, acute renal failure, dermatoses, and rarely angioedema and urticaria. Early supportive management in addition to careful monitoring of urine output and renal function is essential for patients with heart failure, chronic kidney and liver disease, and in patients taking a diuretic after major surgery while taking this medication.

Strongly bound to plasma proteins with approximately 100% bioavailability.

Morniflumate is indicated for the treatment of inflammatory conditions affecting the airways, ENT system, urogenital tract and bone and joint systems in adults. In Italy, morniflumate is also indicated for the treatment of pain associated with ear, nose, throat (ENT) and gastrointestinal inflammatory conditions in children. Morniflumate is a well established NSAID that has been in use for over three decades in Italy (particularly for the treatment of upper respiratory tract infections in children), France, Belgium, Austria, Switzerland, Spain and Portugal; it has a generally favorable tolerability profile.

Morniflumate, given at therapeutic dosages to healthy human volunteers, on leukotriene B4 (LTB4) and thromboxane (TXB2) synthesis, both in purified PMNs (polymorphnuclear neutrophils) and in whole blood. In whole blood experiments, morniflumate reduced blood leukotriene B4 (LTB4) synthesis induced by Ca-ionophore A23187 Bx approximately 50%, both after a single dose and at steady state; the level of inhibition showed a pattern similar to the plasma levels of the bioactive metabolite of morniflumate (M1). The inhibition of serum thromboxane B2 (TXB2) levels was higher than 85%. Hence, morniflumate is demonstrated to reduce arachidonic acid metabolism, by exerting its effects on cyclooxygenase and 5-lipoxygenase. This characteristic might provide a better approach for anti-inflammatory therapy. In several animal models orally administered morniflumate, the beta-morpholinoethyl ester of niflumic acid, proved almost equal to the parent compound in anti-inflammatory, analgesic and antipyretic activity with the absence of gastric irritating/ulcerogenic effects of its acidic parent compound.

0.12 L /kg on average|45 ml/min

The pharmacokinetic availability of niflumic acid in two different pharmaceutical preparations have been studied in 12 subjects after oral administration. Bioavailability and pharmacokinetics studies after oral and intravenous (IV) administration demonstrate that morniflumate is absorbed as from the gastrointestinal tract, followed by rapid hydrolysis in the plasma, releasing the free acidic form, the molecule responsible for its anti-inflammatory effects. The ester displays gastroprotective effect against the ulcerogenic effects of niflumic acid.

2h

The primary mechanism of niflumic acid and its ester is action is inhibition of enzymes involved in the synthesis of inflammatory prostaglandins. This medication inhibits cyclooxygenase and 5-lipoxygenase pathways, which lead to fever and inflammation. Niflumic acid, a calcium-activated Cl- channel blocker, is an analgesic and anti-inflammatory agent used in the treatment of inflammatory conditions. Niflumic acid does directly inhibit calcium channels or activate potassium channels. Niflumic acid selectively reduces noradrenaline- and 5-HT-induced pressor responses by inhibiting a mechanism which leads to the opening of voltage-gated calcium channels. Niflumic acid (NFA) produces biphasic behavior on human CLC-K channels that suggests the presence of two functionally different binding sites: an activating site and a blocking site.

beta-morpholinoethyl niflumate