PicropodophyllinPicropodophyllin
MedChemExpress (MCE)
HY-15494
477-47-4
AXL1717
Picropodophyllotoxin
PPP
99.85%
Powder -20°C 3 years 4°C 2 years In solvent -80°C 1 year -20°C 6 months
Room temperature in continental US
may vary elsewhere.
Picropodophyllin (AXL1717) is a selective insulin-like growth factor-1 receptor (IGF-1R) inhibitor with an IC50 of 1 nM.
Picropodophyllin (AXL1717) (0.5, 2.5, 10 μM) potently inhibits IGF-1-stimulated IGF-1R, Akt (Ser 473) and Erk1/2 phosphorylation in intact cells. Picropodophyllin (AXL1717) also inhibits cell growth, and induces apoptosis in cultured IGF-1R-positive tumor cells[1].Picropodophyllin (AXL1717) synergistically sensitizes HMCL, primary human MM and murine 5T33MM cells to ABT-737 and ABT-199 via further decreasing cell viability and enhancing apoptosis[3]. Picropodophyllin and sorafenib synergistically suppress the proliferation and motility of hepatocellular carcinoma cells[4].
Picropodophyllin (AXL1717) (20 mg/kg/12 h, i.p.) causes complete tumor regression in SCID mice xenografted with human ES-1, BE, and PC3[1]. Picropodophyllin (AXL1717) shows a potent antitumor activity, increases survival in the 5T33MM mouse model[2].
Four to 5-week-old pathogen-free SCID mice are used and housed within plastic isolators in a sterile facility. ES-1, BE, and PC3 cells (all proved to express IGF-1R), or R-v-src (IGF-1R negative) and P12 (overexpressing IGF-1 and IGF-1R), are injected s.c. at 107 cells/mice in a 0.2 mL volume of sterile saline solution. Immunocompetent Balb-c mice are injected with 107JC murine breast cancer cells per mouse in 0.15 mL volume of sterile saline solution. Experimental treatments with Picropodophyllin (AXL1717) (20 mg/kg/12 h) are performed by daily i.p. injections of the compound in 10 μL volume of DMSO: vegetable oil, 10:1 (v/v). Control mice are treated with the vehicle only. Three animals are treated in each group. Tumor growth is measured every second day using vernier calipers, and the tumor volumes are calculated. The mice are carefully observed for the presence of side effects and are sacrificed at the end of the experiments for histological analysis of the lesions. A separate experiment on Picropodophyllin (AXL1717)-treated (systemically and locally) tumor-free mice, including histological analyses of various organs, confirms previous observations that Picropodophyllin (AXL1717) appears to be nontoxic.
IC50: 1 nM (IGF-1R) In Vitro Picropodophyllin (AXL1717) (0.5, 2.5, 10 μM) potently inhibits IGF-1-stimulated IGF-1R, Akt (Ser 473) and Erk1/2 phosphorylation in intact cells. Picropodophyllin (AXL1717) also inhibits cell growth, and induces apoptosis in cultured IGF-1R-positive tumor cells[1].Picropodophyllin (AXL1717) synergistically sensitizes HMCL, primary human MM and murine 5T33MM cells to ABT-737 and ABT-199 via further decreasing cell viability and enhancing apoptosis[3]. Picropodophyllin and sorafenib synergistically suppress the proliferation and motility of hepatocellular carcinoma cells[4]. MedChemExpress (MCE) has not independently confirmed the accuracy of these methods. They are for reference only. 0 --> Picropodophyllin Related Antibodies
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107(2):655-60. Epub 2005 Jul 26. [Content Brief]
[3]. Bieghs L, et al. The IGF-1 receptor inhibitor picropodophyllin potentiates the anti-myeloma activity of a BH3-mimetic. Oncotarget. 2014 Nov 30
5(22):11193-208. [Content Brief]
[4]. Tomizawa M, et al. Picropodophyllin and sorafenib synergistically suppress the proliferation and motility of hepatocellular carcinoma cells. Oncol Lett. 2014 Nov
8(5):2023-2026. Epub 2014 Aug 27. [Content Brief]
[5]. Stromberg T, et al. IGF-1 receptor tyrosine kinase inhibition by the cyclolignan PPP induces G2/M-phase accumulation and apoptosis in multiple myeloma cells. Blood. 2006 Jan 15
107(2):669-78. Epub 2005 Sep 15. [Content Brief]
[6]. Kong YL, et al. Insulin deficiency induces rat renal mesangial cell dysfunction via activation of IGF-1/IGF-1R pathway. Acta Pharmacol Sin. 2016 Feb
37(2):217-27. [Content Brief]
