131959-12-1

Basic information

• Product Name: OKADAOL
• Synonyms: OKADAOL
• CAS NO: 131959-12-1
• Molecular Formula: C44H70O12
• Molecular Weight: 791.02
• Product Categories: Protein phosphatase;Enzyme Inhibitors by Enzyme;P to
• Mol File: 131959-12-1.mol

Chemical Properties

• Boiling Point: 910.5°C at 760 mmHg
• Flash Point: 504.5°C
• Appearance: /
• Density: 1.25g/cm³
• Vapor Pressure: 0mmHg at 25°C
• Refractive Index: 1.58
• Storage Temp.: −20°C
• CAS DataBase Reference: OKADAOL(CAS DataBase Reference)
• NIST Chemistry Reference: OKADAOL(131959-12-1)
• EPA Substance Registry System: OKADAOL(131959-12-1)

Safety Data

• Hazard Codes: Xn
• Statements: 20/21/22-38
• Safety Statements: 26-36
• WGK Germany: 3
• Hazardous Substances Data: 131959-12-1(Hazardous Substances Data)

Usage

InChI:InChI=1/C44H70O12/c1-26-19-36(55-44(21-26)40(48)50-24-32(54-44)22-41(6,49)25-45)28(3)9-10-31-12-16-43(53-31)17-13-35-39(56-43)37(47)30(5)38(52-35)34(46)20-29(4)33-23-42(15-11-27(33)2)14-7-8-18-51-42/h9-10,21,27-29,31-40,45-49H,5,7-8,11-20,22-25H2,1-4,6H3/b10-9+

Upstream product

• 78111-17-8 okadaic acid 

Relevant articles and documents

An analysis of the mechanisms involved in the okadaic acid-induced contraction of the estrogen-primed rat uterus

The contractile effect of okadaic acid (OA) and its derivatives was investigated in the rat uterus. OA (20 μM) induced a transient contraction which, after plateauing, slowly decreased. The structurally related compound okadanol (20 μM) failed to induce any significant contraction. Conversely, the synthetic compound methyl okadaate (20 μM) and the naturally occurring ester 7'-hydroxy-4'-methyl-2'-methylen-hept-4'(E)-enyl okadaate (20 μM) were as active as the free acid. The OA-induced contraction was unaffected in the presence of neomycin (5 mM), mepacrine (30 μM), 1-[N,O-bis(1,5- isoquinolinesulfonyl)-N-methyl-L-tyrosyl]-4-phenylpiperazine (10 μM), calphestin C (3 μM) and 1-(5-isoquinolinylsulfonyl)-2-methylpiperazine (30 μM). The calmodulin inhibitor N-(6-aminohexyl)-5-chloro-1- naphthalenesulfonamide bydrochloride (100 μM) did not modify the amplitude of the OA-induced contraction but significantly increased the rate of tension decay. The myosin light chain kinase inhibitor 1-(5-chloronaphthalene-1- sulfonyl)-1H-hexahydro-1,4-diazepine hydrochloride [1 μM) significantly reduced the peak amplitude of the contraction. Staurosporine (0.03-0.1 μM) did not modify the contractile component of the OA-induced response but inhibited the subsequent decrease in tension. In freshly dispersed myometrial cells loaded with the fluorescent Ca++ indicator indo 1, OA did not produce any significant increase in [Ca++](i). OA (5- to 90-min contact) also failed to modify the intracellular levels of arachidonic acid, compared with basal values. These data suggest that in the rat uterus 1) the contractile effect of OA (20 μM) is specifically mediated by inhibition of protein phosphatases type 1 and/or 2A and is related to a direct interaction with the contractile machinery; 2) the decreasing phase of the OA-induced mechanical response could be mediated by a staurosporine-sensitive protein kinase different from protein kinase C.