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1. 12 Myristoyl 13 Acetylphorbol
2. 12 O Tetradecanoyl Phorbol 13 Acetate
3. 12-myristoyl-13-acetylphorbol
4. 12-o-tetradecanoyl Phorbol 13-acetate
5. 13-acetate, 12-o-tetradecanoyl Phorbol
6. Acetate, Phorbol Myristate
7. Acetate, Tetradecanoylphorbol
8. Myristate Acetate, Phorbol
9. Phorbol 13-acetate, 12-o-tetradecanoyl
10. Phorbol Myristate Acetate
11. Tetradecanoylphorbol Acetate
12. Tetradecanoylphorbol Acetate, 4a Alpha Isomer
13. Tetradecanoylphorbol Acetate, 4a Alpha-isomer
1. 16561-29-8
2. 12-o-tetradecanoylphorbol-13-acetate
3. Phorbol-12-myristate-13-acetate
4. 12-o-tetradecanoylphorbol 13-acetate
5. Phorbol Ester
6. Tetradecanoylphorbol Acetate
7. Factor A1
8. 12-tetradecanoylphorbol 13-acetate
9. Phorbol Myristate Acetate
10. Phorbol 13-acetate 12-myristate
11. Pma
12. Factor A1 (croton Oil)
13. Pma (tumor Promoter)
14. Phorbol 12-tetradecanoate 13-acetate
15. Tpa (phorbol Derivative)
16. Ccris 716
17. Pma (phorbol Ester)
18. Tpa
19. Tpa (phorbol Ester)
20. Phorbol Monoacetate Monomyristate
21. Hsdb 3542
22. 13-o-acetylphorbol 12-myristate
23. 12-o-tetradecanoyl Phorbol Acetate
24. Beta-phorbol 12-myristate 13-acetate
25. Nsc 262244
26. 12-tetradecanoylphorbol 13-monoacetate
27. 4beta-phorbol 12-myristate 13-acetate
28. Phorbol 12-myristate 13-acetate Diester
29. Chembl279115
30. Ni40jaq945
31. Chebi:37537
32. Nsc-262244
33. (1ar,1bs,4ar,7as,7bs,8r,9r,9as)-9a-acetoxy-4a,7b-dihydroxy-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 Tetradecanoate
34. Phorbol 12-myristate 13-acetate (pma)
35. Phorbol Acetate, Myristate
36. 12-o-tetradekanoylphorbol-13-acetat
37. 12-o-tetradecanoyl Phorbol-13-acetate
38. Phorbol-myristate Acetate
39. Mfcd00036736
40. Pentahydroxy-tigliadienone-monoacetate(c)monomyristate(b)
41. Yristate
42. Unii-ni40jaq945
43. 13-tetradecanoylphorbol Acetate
44. Nsc626496
45. Cocarcinogen A1
46. Cocarcinogen C3
47. Phorbol-12-myristate 13-acetate
48. Tetradecanoyl-beta-phorbol Acetate
49. 12-tetradecanoylphorbol-13-acetate
50. 5h-cyclopropa(3,4)benz(1,2-e)azulen-5-one, 1,1a-beta,1b-alpha,4,4a,7a-beta,7b,8,9,9a-decahydro-4a-alpha,7b-beta,9-alpha,9a-beta-tetrahydroxy-3-(hydroxymethyl)-1,1,6,8-beta-tetramethyl-, 9a-acetate 9-myristate
51. 12-o-tetradecanoyl-phorbol-13-acetate
52. 4beta-phorbol-12-myristate-13-acetate
53. Brn 2407201
54. Specplus_000801
55. Spectrum2_001911
56. Spectrum4_000889
57. Spectrum5_001855
58. Molmap_000041
59. Upcmld-dp069
60. 12-o-tetradekanoylphorbol-13-acetat [german]
61. Bidd:pxr0145
62. Cbiol_002014
63. Bspbio_001024
64. Kbiogr_000364
65. Kbiogr_001298
66. Kbioss_000364
67. Spectrum330004
68. Tetradecanoic Acid, 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-yl Ester, (1ar-(1aalpha,1bbeta,4abeta,7aalpha,7balpha,8alpha,9beta,9aalpha))-
69. Divk1c_006897
70. Schembl115567
71. Phorbol12-myristate13-acetate
72. Spbio_001902
73. 1h-cyclopropa[3,4]benz[1,2-e]azulene, Tetradecanoic Acid Deriv.
74. Gtpl2341
75. [acetoxy-dihydroxy-(hydroxymethyl)-tetramethyl-oxo-[?]yl] Tetradecanoate
76. Dtxsid5023798
77. Upcmld-dp069:001
78. Upcmld-dp069:002
79. Bcbcmap01_000182
80. Kbio1_001841
81. Kbio2_000364
82. Kbio2_002932
83. Kbio2_005500
84. Kbio3_000707
85. Kbio3_000708
86. Bio1_000300
87. Bio1_000789
88. Bio1_001278
89. Bio2_000352
90. Bio2_000832
91. Hms1362d05
92. Hms1792d05
93. Hms1990d05
94. Hms3403d05
95. Phorbol 13 Acetate 12 Myristate
96. Ex-a6920
97. Zinc8214783
98. Bdbm50099066
99. Ccg-39863
100. Nsc262244
101. Nsc262644
102. S7791
103. Akos024418767
104. Cs-6053
105. Fs-4842
106. Lmpr0104330002
107. Nsc-262644
108. Nsc-626496
109. Idi1_002107
110. Ncgc00161633-01
111. Ncgc00161633-04
112. Ncgc00161633-05
113. 4-.beta.-phorbol 12-myristate 13-oac
114. Ac-33957
115. Hy-18739
116. Myristic Acid, 9-ester With 1,1aalpha,1bbeta,4,4a,7aalpha,7b,8,9,9a-decahydro-4abeta,7balpha,9beta,9aalpha-tetrahydroxy-3-(hydroxymethyl)-1,1,6,8alpha-tetramethyl-5h-cyclopropa(3,4)benz(1,2-e)azulen-5-one 9a-acetate, (+)-
117. Tetradecanoic 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-yl Ester
118. Tetradecanoic Acid, 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-yl Ester, (1ar-(1aa,1bb,4ab,7aa,7ba, 8a,9b,9aa))-
119. 12-o-tetradecanoylphorbol-13-acetate (tpa)
120. N2060
121. P1585
122. Phorbol-12-tetradecanoyl-13-acetate
123. C05151
124. 4abeta,7aalpha,7balpha,8alpha,9beta,9aalpha)]-
125. Q416716
126. W-201494
127. 12-o-tetradecanoylphorbol-13-acetate [hsdb]
128. Brd-k68552125-001-03-8
129. Brd-k68552125-001-04-6
130. Phorbol 12-myristate 13-acetate Diester [mi]
131. Phorbol-12-myristate-13-acetate - Cas 16561-29-8
132. Phorbol 12-myristate 13-acetate, Synthetic, >=98.0% (tlc)
133. Pma, For Use In Molecular Biology Applications, >=99% (tlc)
134. Phorbol 12-myristate 13-acetate, >=99% (tlc), Film Or Powder
135. 12-o-tetradecanoyl Phorbol-13-acetate;cocarcinogen A1; Cocarcinogen C3
136. (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-yl Tetradecanoate
137. (1s,2s,6r,10s,11r,13s,14r,15r)-13-(acetyloxy)-1,6-dihydroxy-8-(hydroxymethyl)-4,12,12,15-tetramethyl-5-oxotetracyclo[8.5.0.0^{2,6}.0^{11,13}]pentadeca-3,8-dien-14-yl Tetradecanoate
138. [(1s,2s,6r,10s,11r,13s,14r,15r)-13-acetyloxy-1,6-dihydroxy-8-(hydroxymethyl)-4,12,12,15-tetramethyl-5-oxo-14-tetracyclo[8.5.0.02,6.011,13]pentadeca-3,8-dienyl] Tetradecanoate
139. 11016-13-0
140. 5h-cyclopropa(3,4)benz(1,2-e)azulen-5-one, 1,1a-beta,1b-alpha,4,4a,7a-beta,7b,8,9,9a-decahydro-4a-alpha,7b-beta,9-alpha,9a-beta-tetrahydroxy-3-(hydroxymethyl)-1,1,6,8-beta-tetramethyl-, 9a-acetate 9-m
141. Myristic Acid, 9-ester With 1,1a-alpha,1b-beta,4,4a,7a-alpha,7b,8,9,9a-decahydro-4a-beta,7b-alpha,9-beta,9a-alpha-tetrahydroxy-3-(hydroxymethyl)-1,1,6,8-alpha-tetramethyl-5h-cyclopropa(3,4)benz(1,2-e)azulen-5-one, 9a-acetate
142. Myristic Acid, 9-ester With 1,1aalpha,1bbeta,4,4a,7aalpha,7b,8,9,9a-decahydro-4abeta,7balpha,9beta,9aalpha-tetrahydroxy-3-(hydroxymethyl)-1,1,6,8alpha-tetramethyl-5h-cyclopropa[3,4]benz[1,2-e]azulen-5
143. Tetradecanoic 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
144. Tetradecanoic Acid, 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-yl Ester, [1ar-(1aalpha,1bbeta,
145. Tetradisant-[[4-(1, 1-oxideomega.-[2-(dodecylthio)ethoxy]-,10-tetrahydro-6,8,11-trihydroxy-1-methoxy-, (8s-cis)-, Mixt. With Denatured Calf Thymus Dnaa, (2s-cis)-, Compd. With Sulfinylbis[methane] (2:1)2s-cis)-1:9)
| Molecular Weight | 616.8 g/mol |
|---|---|
| Molecular Formula | C36H56O8 |
| XLogP3 | 6.5 |
| Hydrogen Bond Donor Count | 3 |
| Hydrogen Bond Acceptor Count | 8 |
| Rotatable Bond Count | 17 |
| Exact Mass | 616.39751874 g/mol |
| Monoisotopic Mass | 616.39751874 g/mol |
| Topological Polar Surface Area | 130 Ų |
| Heavy Atom Count | 44 |
| Formal Charge | 0 |
| Complexity | 1150 |
| Isotope Atom Count | 0 |
| Defined Atom Stereocenter Count | 8 |
| Undefined Atom Stereocenter Count | 0 |
| Defined Bond Stereocenter Count | 0 |
| Undefined Bond Stereocenter Count | 0 |
| Covalently Bonded Unit Count | 1 |
/CLINICAL TRIALS/ ClinicalTrials.gov is a registry and results database of publicly and privately supported clinical studies of human participants conducted around the world. The Web site is maintained by the National Library of Medicine (NLM) and the National Institutes of Health (NIH). Each ClinicalTrials.gov record presents summary information about a study protocol and includes the following: Disease or condition; Intervention (for example, the medical product, behavior, or procedure being studied); Title, description, and design of the study; Requirements for participation (eligibility criteria); Locations where the study is being conducted; Contact information for the study locations; and Links to relevant information on other health Web sites, such as NLM's MedlinePlus for patient health information and PubMed for citations and abstracts for scholarly articles in the field of medicine. 12-O-Tetradecanoylphorbol-13-acetate is included in the database.
NIH/NLM; ClinicalTrials.Gov. Available from, as of March 17, 2016: https://clinicaltrials.gov/ct2/results?term=12-O-TETRADECANOYLPHORBOL-13-ACETATE&Search=Search
/EXPL THER/ Phorbol esters activate protein kinase C and modulate a variety of downstream cell signaling pathways. 12-O-tetradecanoylphorbol-13-acetate (TPA) is a phorbol ester that induces differentiation or apoptosis in a variety of cell lines at low concentrations. A phase I dose escalation trial of TPA was undertaken for patients with relapsed or refractory malignancies. The starting dose was 0.063 mg/sq m and most patients were treated with an intravenous infusion of TPA on days 1-5 and 8-12 followed by a 2-week rest period prior to retreatment. Thirty-five patients were treated. A biological assay was used to monitor levels of TPA-like activity in the blood after treatment. Serious adverse events included individual episodes of gross hematuria, a grand mal seizure, syncope, and hypotension. Many patients had transient fatigue, mild dyspnea, fever, rigors, and muscular aches shortly after the infusion. Dose-limiting toxicities included syncope and hypotension at a dose of 0.188 mg/sq m. Only a single patient had evidence of tumor response. These studies establish 0.125 mg/sq m as the maximally tolerated dose when TPA is administered on this schedule.
PMID:16231182 Schaar D et al; Cancer Chemother Pharmacol 57 (6): 789-95 (2006)
Carcinogens
Substances that increase the risk of NEOPLASMS in humans or animals. Both genotoxic chemicals, which affect DNA directly, and nongenotoxic chemicals, which induce neoplasms by other mechanism, are included. (See all compounds classified as Carcinogens.)
...Mouse skin localization expt...determined that at 3-6 hr after skin application /with tritiated PMA/ the keratin layer just above basal cells was highly labeled, & sebaceous glands & hair follicles were moderately labeled. After 48 hr there was still some labeling in sebaceous glands & hair follicles. Half-life of...promoter was close to 24 hr.
Searle, C. E. (ed.). Chemical Carcinogens. ACS Monograph 173. Washington, DC: American Chemical Society, 1976., p. 38
...the major pathway in the metabolism of TPA is the hydrolysis of the two ester groups, ... in the rodent skin model all hydrolytic products lack tumor promoting activity, the major toxicological effect of TPA. The metabolic hydrolysis requires the activity of esterases, the activity of which differs between tissues and species. ... both ester groups of TPA can be hydrolysed in mouse skin and in cultured cells, giving rise to the monoesters 12-tetradecanoylphorbol and phorbol-13-acetate, as well as the product of complete hydrolysis, i.e. phorbol. Reduction of the keto group at C-3 was identified as a further metabolic pathway in mouse skin. ... Noteworthy, no other metabolites were detected in the microsomal incubations, suggesting that cytochrome 450-mediated oxidative metabolism is not involved in TPA metabolism. Ester group hydrolysis was also the only metabolic reaction observed in various cultured cells ... .
EFSA Journal 13 (12): 4321 (2015)
... the hydrolysis of TPA paralleled the loss of activity for induction of ornithine decarboxylase (ODC). As ODC is a marker for tumor promotion, these findings suggest that all three hydrolytic metabolites of TPA (the two monoesters and phorbol) are devoid of tumor promoting activity. Marked differences in the rate of hydrolysis of TPA and a structural analogue, phorbol-12,13-didecanoate (PDD) were observed between cultured fibroblasts from various animal species, suggesting that the hydrolytic metabolism of phorbol diesters depends on the cell type and on the chemical structure of the diester ... .
EFSA Journal 13 (12): 4321 (2015)
... the metabolism of radiolabeled TPA /was studied/ in the back skin of mice in vivo. In addition to hydrolytic metabolites, several novel lipophilic metabolites were detected and identified as TPA esterified with long chain fatty acids at the C-20 hydroxyl group. These TPA-20-acylates appeared to be devoid of tumor promoting activity but were partly hydrolysed back to TPA in mouse skin ... .
EFSA Journal 13 (12): 4321 (2015)
The few in vitro metabolism studies of TPA involving human cells indicate that many human cell lines in culture do not metabolize TPA to an appreciable extent ... .
EFSA Journal 13 (12): 4321 (2015)
... after /mouse/ skin application /with tritiated PMA/... Half-life of ... promoter was close to 24 hr.
Searle, C. E. (ed.). Chemical Carcinogens. ACS Monograph 173. Washington, DC: American Chemical Society, 1976., p. 38
A terminal half-life of 11 +/- 3.9 hours was calculated (from five infusions in four patients) ... .
EFSA Journal 13 (12): 4321 (2015)
The tumor promoter, 12-O-tetradecanoylphorbol-13-acetate (TPA), has a differential role on the regulation of the cell cycle in a variety of tumor cells. The mechanism between TPA and the cell cycle in breast cancer is not fully understood. Therefore, we investigated the regulatory mechanism of TPA on control of the cell cycle of breast cancer cells. Our results showed that TPA increased the level of p21 expression in MCF-7 cells with wild-type p53 and MDA-MB-231 cells with mutant p53 in a dose-dependent manner. In contrast, TPA decreased the expression of p53 in MCF-7 cells, but did not affect MDA-MB-231 cells. We next examined the regulatory mechanism of TPA on p21 and p53 expression. Our results showed that the TPA-induced up-regulation of p21 and down-regulation of p53 was reversed by UO126 (a MEK1/2 inhibitor), but not by SP600125 (a JNK inhibitor) or SB203580 (a p38 inhibitor), although TPA increased the phosphorylation of ERK and JNK in MCF-7 cells. In addition, the TPA-induced arrest of the G2/M phase was also recovered by UO126 treatment. To confirm the expression of p21 through the MEK/ERK pathway, cells were transfected with constitutively active (CA)-MEK adenovirus. Our results showed that the expression of p21 was significantly increased by CA-MEK overexpression. Taken together, we suggest that TPA reciprocally regulates the level of p21 and p53 expression via a MEK/ERK-dependent pathway. The up-regulation of p21 in response to TPA is mediated through a p53-independent mechanism in breast cancer cells.
PMID:22020547 Han J et al; Oncol Rep 27 (2): 517-22 (2012)
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