DC Chemicals · Product datasheet

Phorbol 12-myristate 13-acetate (PMA) — Datasheet

CAT. NO. DC10645

Product page and current package options

ParameterValue
Chemical NamePhorbol 12-myristate 13-acetate
CAS No.16561-29-8
SynonymsTetradecanoic acid,(1aR,1bS,4aR,7aS,7bS,8R,9R,9aS)-9a-(acetyloxy)-1a,1b,4,4a,5,7a,7b,8,9,9a-decahydro-4a,7b-dihydroxy-3-(hydroxymethyl)-1,1,6,8-tetramethyl-5-oxo-1H-cyclopropa[3,4]benz[1,2-e]azulen-9-ylester;12-O-tetradecanoyl phorbol-13-acetate;4β-Phorbol 12-Myristate 13-Acetate;Invivogen;PHORBOL 12-MYRISTATE 13-ACETATE;PMA;PMA (TPA,Cocarcinogen A1,12-O-Tetradecanoyl-phorbol 13-Acetate,Phorbol 12-myristate 13-acetate);Tetradecanoic acid,(1aR,1bS,4aR,7aS,7bS,8R,9R,9aS)-9a-(acetyloxy)-1a,1b,4,4a,5,7a,7b,8,9,9a-de...;12-O-Tetradecanoylphorbol 13-acetate;4β,9α,12β,13α,20-Pentahydroxytiglia-1,6-dien-3-one 12-tetradecanoate 13-acetate;TPA;12-o-tetradecanoyl phorbol acetate;factora1;Cocarcinogen A1;Cocarcinogen C3;pma(tumorpromoter);factora1[crotonoil];factora1(crotonoil);phorbolmyristateacetate;phorbolacetate,myristate;12-O-Tetradecanoylphorbol-13-acetate;,9aalpha))-;Factor A1;Phorbol myristate acetate;Factor A1 (croton oil);Phorbol ester;Tetradecanoylphorbol acetate;PMA (tumor promot
FormulaC36H56O8
M.Wt616.8251
SMILESO(C(C([H])([H])[H])=O)[C@@]12[C@@]([H])([C@@]([H])(C([H])([H])[H])[C@@]3([C@]4([H])C([H])=C(C([H])([H])[H])C([C@]4(C([H])([H])C(C([H])([H])O[H])=C([H])[C@@]3([H])[C@]1([H])C2(C([H])([H])[H])C([H])([H])[H])O[H])=O)O[H])OC(C([H])([H])C([H])([H])C([H])([H])C([H])([H])C([H])([H])C([H])([H])C([H])([H])C([H])([H])C([H])([H])C([H])([H])C([H])([H])C([H])([H])C([H])([H])[H])=O
Purity>98%
Storage2 years -20°C Powder, 2 weeks 4°C in DMSO, 6 months -80°C in DMSO

Biological Activity

Phorbol 12-myristate 13-acetate (PMA), a phorbol ester, is a commonly used PKC activator.

In Vitro

In order to examine the role of PKC in p38MAPK phosphorylation, the cells are stimulated with the PKC activator, PMA (100 nM), which mimics the binding of DAG, the natural activator of PKC, to the C1 region of the PKCs. p38MAPK phosphorylation by PMA is observed in the two cell types similar to that observed by GnRH in αT3-1 cells, that is, a slow sustained activation (3.2-fold and 3.6-fold, respectively at 30 min). The paradoxical findings that PKCs activated by GnRH and PMA play a differential role in p38MAPK phosphorylation may be explained by differential localization of the PKCs. Basal, GnRH- and PMA- stimulation of p38MAPK phosphorylation in αT3-1 cells is mediated by Ca2+ influx via voltage-gated Ca2+ channels and Ca2+ mobilization, while in the differentiated LβT2 gonadotrope cells it is mediated only by Ca2+ mobilization[2].

In Vivo

PMA is a PKC agonist, which reverses the damage induced by 5-hydroxydecanoic acid (5-HD). Thus, activation of the mitoKATP protected mitochondrial function in SOD and MDA via the PKC pathway[3].

References & source

DC Chemicals original product information

Published experimental findings depend on the model and assay conditions. They do not guarantee equivalent performance in every application. For laboratory research use only.

Cart

Request quotation