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Phorbol 12-myristate 13-acetate

Phorbol 12-myristate 13-acetate
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Purity:100%
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Phorbol 12-myristate 13-acetate

Catalog No. TQ0198Cas No. 16561-29-8
Phorbol 12-myristate 13-acetate (PMA) belongs to the phorbol ester group of natural products and is an activator of PKC, SphK, and NF-κB. Phorbol 12-myristate 13-acetate induces THP1 cell differentiation.
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Pack SizePriceAvailabilityQuantity
1 mg$40$50In Stock
5 mg$71.2$89In Stock
10 mg$103.2$129In Stock
25 mg$170.4$213In Stock
50 mg$252$315In Stock
1 mL x 10 mM (in DMSO)$98.4$123In Stock
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Product Introduction

Bioactivity
Description
Phorbol 12-myristate 13-acetate (PMA) belongs to the phorbol ester group of natural products and is an activator of PKC, SphK, and NF-κB. Phorbol 12-myristate 13-acetate induces THP1 cell differentiation.
In vitro
METHODS: Sphere-cultured human melanoma cells WM series were treated with Phorbol 12-myristate 13-acetate (50 ng/mL) for 3 days, and cell growth was examined using the MTS.
RESULTS: Phorbol 12-myristate 13-acetate promoted the proliferation of melanoma cells, and the cell number of WM35 cells increased to 265%. [1]
METHODS: Human mononuclear leukocytes THP-1 were treated with Phorbol 12-myristate 13-acetate (200 ng/mL) for 1-5 days, and morphology was assessed using light microscopy and target expression was detected using Flow Cytometry.
RESULTS: Phorbol 12-myristate 13-acetate induced THP-1 cells to differentiate into macrophage-like cells (THP-1 macrophages). Cell surface expression of CD11 and CD14 was increased. [2]
METHODS: Human venous endothelial cells HUVECs were treated with Phorbol 12-myristate 13-acetate (10-40 ng/mL) for 8 h. Cell migration was detected using the Wound healing migration assay.
RESULTS: Short-term treatment with Phorbol 12-myristate 13-acetate enhanced endothelial cell migration. [3]
In vivo
METHODS: To investigate the effects of phorbol esters on rodent brain development, Phorbol 12-myristate 13-acetate (100-500 μg/kg) was administered as a single intraperitoneal injection to neonatal rats and mice deficient in IL-18 or IRAK-4, and the animals were necropsied 24 h, 7 days, or 14 days later.
RESULTS: Phorbol 12-myristate 13-acetate induced an inflammatory response and extensive neurodegeneration in the brain. Lack of IL-18 or IRAK-4 protected against Phorbol 12-myristate 13-acetate-induced brain damage. [4]
METHODS: To construct an acute mouse ear inflammation model, both ears of CD-1 mice were treated topically with Phorbol 12-myristate 13-acetate (20 μL of 125 μg/mL PMA acetone solution), air-dried and completely absorbed.
RESULTS: Ear tissues attacked with Phorbol 12-myristate 13-acetate began to show signs of inflammation, including swelling and redness, approximately 2 hours after application. [5]
Cell Research
αT3-1 and LβT-2 cells are grown in monolayer cultured in DMEM in humidified incubator 5% CO2 at 37°C. Serum starvation is with 0.1% FCS in the same medium for 16 h. GnRH and PMA are then added for the length of time as indicated. In general, αT3-1 cells are transiently transfected by ExGen 500 or by jetPRIME, while LβT2 cells only by jetPRIME transfection reagent. For experiments with dominant-negative (DN) PKCs, αT3-1 cells (in 6 cm plates) are transfected with 1.5 μg of p38α-GFP with 3 μg of control vector, pCDNA3, or with 3 μg of the DN-PKCs constructs. For LβT2 cells, transfections are performed (in 10 cm plates) with 4 μg of p38α-GFP along with 9 μg of control vector, pCDNA3, or with 9 μg of the DN-PKCs constructs. Approximately 30 h after transfection, the cells are serum-starved (0.1% FCS) for 16 h and later stimulated with GnRH or PMA, washed twice with ice-cold PBS, treated with the lysis buffer, followed by one freeze-thaw cycle. Cells are harvested; following centrifugation (15,000×g, 15 min, 4°C) supernatants are taken for immunoprecipitation experiments [2].
Animal Research
All experiments are performed with male Wistar rats (weighing 250-280 g). One hundred and thirty-five Wistar rats are randomly divided into seven groups. (1) Rats in the sham group (n=21) are given a lateral cerebral ventricle injection of 0.9% normal saline; (2) Rats in the IR group (n=21) are given a lateral cerebral ventricle injection of 0.9% normal saline 30 min before middle cerebral artery occlusion (MCAO); (3) Rats in the Carbenoxolone (CBX) group (n=21) are given a lateral cerebral ventricle injection of CBX (5 μg/mL×10 μL) 30 min before MCAO; (4) Rats in the Sch-6783 group (n=21) are given a lateral cerebral ventricle injection of DZX (2 mM×30 μL) 30 min prior to MCAO; (5) Rats in the 5-HD group (n=21) are given a lateral cerebral ventricle injection of 5-HD (100 mM×10 μL), and after 10 min, DZX is injected 15 min prior to MCAO; (6) The rats in the DZX + Ro group (n=15) are given a lateral cerebral ventricle injection of DZX, and after 10 min, Ro-31-8425 (400 μg/kg) is injected 15 min prior to MCAO; (7) The rats in the 5-HD+PMA group (n=15) are given an intraperitoneal injection of PMA (200 μg/kg) after the injection of 5-HD and DZX [3].
AliasPMA
Chemical Properties
Molecular Weight616.83
FormulaC36H56O8
Cas No.16561-29-8
Storage & Solubility Information
Storagekeep away from direct sunlight Powder: -20°C for 3 years | In solvent: -80°C for 1 year
Solubility Information
DMSO: 60 mg/mL (97.27 mM)
H2O: Insoluble
5% DMSO+95% Saline: 2.5 mg/mL (4.05 mM, precipitation)
Solution Preparation Table
DMSO/5% DMSO+95% Saline
1mg5mg10mg50mg
1 mM1.6212 mL8.1060 mL16.2119 mL81.0596 mL
DMSO
1mg5mg10mg50mg
5 mM0.3242 mL1.6212 mL3.2424 mL16.2119 mL
10 mM0.1621 mL0.8106 mL1.6212 mL8.1060 mL
20 mM0.0811 mL0.4053 mL0.8106 mL4.0530 mL
50 mM0.0324 mL0.1621 mL0.3242 mL1.6212 mL
100 mM0.0162 mL0.0811 mL0.1621 mL0.8106 mL

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