33705-05-4

Upstream product

• 108-24-7 acetic anhydride 
• 64180-95-6 C₃₂H₄₂O₇ 
• 64180-95-6 (2Z,4E,6E)-Deca-2,4,6-trienoic acid (1aR,1bS,4aR,7aS,7bR,8R,9R,9aS)-9a-acetoxy-7b-hydroxy-3-hydroxymethyl-1,1,6,8-tetramethyl-5-oxo-1a,1b,4,4a,5,7a,7b,8,9,9a-decahydro-1H-cyclopropa[3,4]benzo[1,2-e]azulen-9-yl ester 
• 64181-00-6 Acetic acid (1aR,1bS,4aS,7aR,7bS,8R,9R,9aS)-5,9-diacetoxy-3-acetoxymethyl-7b-hydroxy-1,1,6,8-tetramethyl-1,1a,1b,4,4a,5,7a,7b,8,9-decahydro-cyclopropa[3,4]benzo[1,2-e]azulen-9a-yl ester 
• 64181-01-7 Acetic acid (1aR,1bS,4aS,7aR,7bS,8R,9R,9aS)-9-acetoxy-3-acetoxymethyl-5,7b-dihydroxy-1,1,6,8-tetramethyl-1,1a,1b,4,4a,5,7a,7b,8,9-decahydro-cyclopropa[3,4]benzo[1,2-e]azulen-9a-yl ester 
• 22338-57-4 isophorbol 12,13,20-triacetate 

Relevant academic research and scientific papers

Major skin-irritant principle from Synadenium grantii

The latex of Synadenium grantii Hook F. (Euphorbiaceae) yielded a novel skin irritant, 12-O-tigloyl-4-deoxyphorbol-13-isobutyrate (I). The identity of the diterpene parent alcohol and the relative positions of the esterifying groups were established by spectral analysis and experiments leading to the hydrolysis and acetylation of I. Compound I is the first phorbol derivative to be reported from the genus Synadenium.

Inhibition of cytopathic effect of human immunodeficiency virus type-1 by various phorbol derivatives

Forty-eight derivatives of phorbol (9) and isophorbol (14) were evaluated for their inhibition of human immunodeficiency virus (HIV)-1 induced cytopathic effects (CPE) on MT-4 cells, as well as their activation of protein kinase C (PKC), as indices of anti-HIV-1 and tumor promoting activities, respectively. Of these compounds, the most potent inhibition of CPE was observed in 12-O-tetradecanoylphorbol 13-acetate (8) and 12-O-acetylphorbol 13-decanoate (6). The former also showed the strongest PKC activation activity, while the latter showed no activity at 10 ng/ml. Both activities were generally observed in those phorbol derivatives with an A/B trans configuration, but not in the isophorbol derivatives with an A/B cis configuration. Acetylation of 20-OH in the phorbol derivatives significantly reduced the inhibition of CPE, as shown in 12-O-, 20-O-diacetylphorbol 13-decanoate (6a) (IC100=15.6 μg/ml) vs. compound 6 (IC100=0.0076 μg/ml), and 12-O-tetradecanoylphorbol 13,20-diacetate (8a) (IC100=15.6 μg/ml) vs. 12-O- tetradecanoylphorbol 13-acetate (8) (IC100=0.00048 μg/ml), except in the case of 12-O-decanoylphorbol 13-(2-methylbutyrate) (4) and phorbol 12,13-diacetate (9c). The reduction of a carbonyl group at C-3 abruptly reduced the inhibition of CPE, as observed in 3β-hydroxyphorbol 12,13,20-triacetate (9f) (IC100=500 μg/ml) vs. phorbol 12,13,20-triacetate (9d) (IC100=62.5 μg/ml). Although 8 was equipotent in the inhibition of CPE, and activation of PKC, both activities were abruptly decreased by the acetylation of 20-OH and methylation of 4-OH [as in 8a and 4-O-methyl-12-O- tetradecanoylphorbol 13,20-diacetate (8b), respectively]. On the other hand, its positional isomer (12-O-acetylphorbol 13-tetradecanoate (8c) showed neither activities. The removal of a long acyl group in 8 led to a substantial loss of both activities, as shown in phorbol 13-acetate (9b). Of the 12-O-acetyl-13-O-acylphorbol derivatives, the highest inhibition of CPE was observed in 6, which has a dodecanoyl residue at C-13. Both an increase and decrease in the number of fatty acid carbon chains resulted in significant reduction of the inhibition of CPE.