Bendazac

282.29

282.29

243-569-2

G4AG71204O

DTXSID1048334

M - Musculo-skeletal system|S - Sensory organs

2933990090

64.4

3.1

white to off-white crystalline powder

1.3±0.1 g/cm3

160 °C

508.2°C at 760 mmHg

261.1±25.9 °C

1.630

3.78E-11mmHg at 25°C

Oral-rat LD50: 1200 mg/kg; Oral-Mouse LD50: 1105 mg/kg

Flammable; burning produces toxic nitrogen oxide fumes

AF5085000

Ventilated, low temperature and dry

P264, P270, P301+P312, P330, P501

H302

|Warning|H302 (100%): Harmful if swallowed [Warning Acute toxicity, oral]|P264, P270, P301+P312, P330, and P501|Aggregated GHS information provided by 2 companies from 1 notifications to the ECHA C&L Inventory.

moderately toxic

A number of case reports demonstrating the capability for bendazac oral and eye drop therapy to cause potential hepatotoxicity via increases in serum transaminases in patients have been documented. Moreover, bendazac has also since been discontinued or withdrawn in various international regions due to the possibility and risk of eliciting hepatotoxicity in patients.

Bendazac is >99% highly bound to plasma albumin protein in healthy subjects.

Prior to the withdrawal of bendazac from various international regions of use due to concerns for hepatotoxicity the chemical had demonstrated potential usefulness predominantly as the prescription medication bendazac lysine for the indication of managing the level of vision in patients with mild to moderate cataracts to facilitate delaying the need for surgical intervention. Elsewhere bendazac may still be available in a limited capacity as a non-prescription topical cream product for treating conditions like local pain, inflammation, dermatitis, eczema, pruritis, hives, insect bites, burns, erythema, and others - although such products may also be facing general discontinuation.

Bendazac principally demonstrates an antidenaturant action on proteins. This effect has been shown to inhibit the denaturation of various proteins like ocular lens proteins by heat, ultraviolet radiation, free radicals, and other chemicals. The medication may be administered to patients via a number of different formulations, including orally as the lysine salt, as eye drops, or even topical applications for the skin. Some preliminary studies have suggested that an apparent improvement of the blood-retinal barrier had been observed in diabetic patients using bendazac lysine 500 mg three times a day for three to six months. Moreover, the use of topical bendazac has also been shown to demonstrate anti-inflammatory effects in animal models and clinical studies to effectively treat varied dermatoses, especially those involving a necrotic component. Additionally, bendazac has also demonstrated choleretic and antilipidaemic activities that have resulted in substantial reductions in beta/alpha lipoprotein ratio, and total lipid, total cholesterol, and triglyceride levels in patients with dyslipidaemia using oral bendazac lysine 500 mg three times daily. The medication has also elicited the inhibition of phytohaemagglutinin induced lymphocyte transformation in vitro.

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.)

Administered as its lysine salt, a 500 mg oral tablet of bendazac is well absorbed into the human body with maximum plasma concentrations Cmax ranging from 35 to 55 mg/L being attained within 0.5 to 1 hour in healthy volunteers after oral administration of a single 500 mg dose.|About 60% of a dose of bendazac is eliminated via the urine as its primary metabolite, 5-hydroxybendazac. Approximately 15% of a dose is eliminated as unchanged drug and bendazac glucuronide in the urine as well.|The volume of distribution documented for bendazac is 0.16 L/kg.|The plasma clearance recorded for bendazac is given as 0.018 to 0.054 L/h/kg with a mean of 0.033 L/h/kg.

Bendazac is largely eliminated by metabolism, where more than 60% of an administered dose is excreted in the urine as the hydroxylated primary metabolite 5-hydroxybendazac and its glucuronide while up to approximately 15% of a bendazac dose is also excreted in the urine unchanged and as a glucuronide. Unfortunately, there is little data available regarding the specific enzymes responsible for bendazac's metabolism.

The plasma elimination half-life recorded for bendazac is given as 1.7 to 5.2 hours, with a mean of 3.5 hours.

Bendazac seems to elicit an anticataract action by inhibiting the denaturation of ocular lens proteins, although the precise mechanisms by which this action occurs has not yet been formally elucidated - despite there being many proposed mechanisms. In particular, the denaturation of lens proteins may in part be prevented by inhibiting the binding of certain chemicals like cyanates or sugars and 5-hydroxybendazac - the major metabolite of bendazac - has been shown to be capable of inhibiting the glycosylation of lens proteins by sugars like galactose or glucose-6-phosphate in a dose-dependent manner. Moreover, the apparent ability for administered bendazac to elicit free radical scavenger activities due to interactions with protein molecules suggests that the medication may also be able to prevent the oxidation of lens proteins by free radicals in the development of cataracts. Furthermore, bendazac may also be capable of reducing the sulfhydryl group oxidation of lens proteins by the saliva, serum, or urine from patients with cataracts following single dose administration and reduce biological liquid oxidant activity (BLOA) in doing so. Otherwise, it is believed that bendazac also possesses non-steroidal anti-inflammatory actions, as well as analgesic, antipyretic, and platelet-inhibitory effects These effects may be accounted for in part by the substance's capability to inhibit prostaglandin synthesis by inhibiting cyclooxygenase activity in converting arachidonic acid to cyclic endoperoxides - the precursors of prostaglandins.

bendazac