1. Bendazolic Acid
2. Bendazolic Acid, Sodium Salt
2. Bendazolic Acid
4. 2-(1-benzyl-1h-indazol-3-yloxy)acetic Acid
10. 1-benzylindazole-3-oxyacetic Acid
11. 2-((1-benzyl-1h-indazol-3-yl)oxy)acetic Acid
12. Af 983
13. ((1-(phenylmethyl)-1h-indazol-3-yl)oxy)acetic Acid
14. Einecs 243-569-2
15. ((1-benzyl-1h-indazol-3-yl)oxy)acetic Acid
17. Brn 0893958
18. [(1-benzyl-1h-indazol-3-yl)oxy]acetic Acid
19. Acetic Acid, [[1-(phenylmethyl)-1h-indazol-3-yl]oxy]-
20. Af 1934 [lysine]
24. Acetic Acid, ((1-benzyl-1h-indazol-3-yl)oxy)-
25. Bindazac; Dogalina; Zildasac; Zildazac
26. Acetic Acid, ((1-(phenylmethyl)-1h-indazol-3-yl)oxy)-
27. 2-[(1-benzyl-1h-indazol-3-yl)oxy]acetic Acid
28. [[1-(phenylmethyl)-1h-indazol-3-yl]oxy]acetic Acid
30. Bendazacum [inn-latin]
31. Bendazaco [inn-spanish]
32. 2-(1-benzylindazol-3-yl)oxyacetic Acid
34. Bendazac [usan:inn:ban:jan]
35. Iwazac (tn)
36. Bendaline (salt/mix)
37. Bendazac [usan]
38. Bendazac [inn]
39. Bendazac [jan]
40. Bendazac [mi]
41. Bendazac [mart.]
42. Bendazac [who-dd]
43. Bendazac Lysine (salt/mix)
45. Af-1934 Lysine
46. Bendazac (jan/usan/inn)
48. 5-23-11-00246 (beilstein Handbook Reference)
49. Af 1934 (salt/mix)
50. Af 1934 Free Acid
51. Af-1934 Free Acid
53. Bendazac, >=98% (hplc)
65. [(1-benzyl-3-indazolyl)oxy]acetic Acid
74. [(1-benzyl-1h-indazol-3-yl)-oxy]acetic Acid
79. Acetic Acid, 2-[[1-(phenylmethyl)-1h-indazol-3-yl]oxy]-
80. 2-(1-benzylindazol-3-yl)oxyacetic Acid;2-(1-benzyl-1h-indazol-3-yloxy)acetic Acid
81. Acetic Acid, ((1-(phenylmethyl)-1h-indazol-3-yl)oxy)- (2) ((1-benzyl-1h-indazol-3-yl)oxy)acetic Acid.
|Molecular Weight||282.29 g/mol|
|Hydrogen Bond Donor Count||1|
|Hydrogen Bond Acceptor Count||4|
|Rotatable Bond Count||5|
|Exact Mass||282.10044231 g/mol|
|Monoisotopic Mass||282.10044231 g/mol|
|Topological Polar Surface Area||64.4 Å²|
|Heavy Atom Count||21|
|Isotope Atom Count||0|
|Defined Atom Stereocenter Count||0|
|Undefined Atom Stereocenter Count||0|
|Defined Bond Stereocenter Count||0|
|Undefined Bond Stereocenter Count||0|
|Covalently Bonded Unit Count||1|
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, Non-Steroidal
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.)
M - Musculo-skeletal system
M02 - Topical products for joint and muscular pain
M02A - Topical products for joint and muscular pain
M02AA - Antiinflammatory preparations, non-steroids for topical use
M02AA11 - Bendazac
S - Sensory organs
S01 - Ophthalmologicals
S01B - Antiinflammatory agents
S01BC - Antiinflammatory agents, non-steroids
S01BC07 - Bendazac
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.
Route of Elimination
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.
Volume of Distribution
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.