Miltefosine (Synonyms: Hexadecylphosphocholine, HPC, NSC 605583) |
| Catalog No.GC10811 |
PI3K/Akt inhibitor
Products are for research use only. Not for human use. We do not sell to patients.
Cas No.: 58066-85-6
Sample solution is provided at 25 µL, 10mM.
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Miltefosine is an inhibitor of PI3K/Akt signaling with IC50 value of 34.6±11.7μM, 6.8±0.9 μM when tested with MCF7 and Hela-WT respectively [1].
PI3K (phosphoinositide-3-kinase) family is an important part in the growth factor super-family signaling process, and can be activated by a variety of cytokines and chemical factors. The activation of PI3K can phosphorylate and activate AKT, localizing it in the plasma membrane. The PI3K/Akt pathway is an intracellular signaling pathway which plays an important role in regulating cell cycle, such as cellular quiescence, proliferation, cancer, longevity and so forth [2, 3]. Many studies have shown that PI3K/Akt had abnormal expression in patients with cancer or virus infection.
Miltefosine is an inhibitor for PI3K/Akt signaling. When tested with macrophages infected by human HIV-1 virus, miltefosine showed significant ability to reduce the viral production via inhibiting PI3K/Akt signaling pathway [4]. In L6E9 skeltal muscle cell line, treatment of milefosine resulted in the resistance of skeletal muscle cells via inhibiting PI3K/Akt signaling pathway [5].
References:
[1]. Rybczynska, M., et al., MDR1 causes resistance to the antitumour drug miltefosine. Br J Cancer, 2001. 84(10): p. 1405-11.
[2]. Bauer, T.M., M.R. Patel, and J.R. Infante, Targeting PI3 kinase in cancer. Pharmacol Ther, 2015. 146c: p. 53-60.
[3]. Minami, A., et al., Connection between Tumor Suppressor BRCA1 and PTEN in Damaged DNA Repair. Front Oncol, 2014. 4: p. 318.
[4]. Chugh, P., et al., Akt inhibitors as an HIV-1 infected macrophage-specific anti-viral therapy. Retrovirology, 2008. 5(11): p. 1742-4690.
[5]. Verma, N.K. and C.S. Dey, The anti-leishmanial drug miltefosine causes insulin resistance in skeletal muscle cells in vitro. Diabetologia, 2006. 49(7): p. 1656-60.
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