Tuesday 23 April 2019 - 01:02
In Business 39 Years - Since 1980
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I-3344 INK128, Free Base, >99%
Synonyms : [MLN0128] [Sapanisertib]
- Size
- US $
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- £
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- 1 mg
- 32
- 28
- 24
- 3,600
- In stock
- 5 mg
- 64
- 56
- 49
- 7,200
- In stock
- 10 mg
- 88
- 78
- 67
- 9,800
- In stock
- 25 mg
- 155
- 137
- 119
- 17,300
- In stock
- 50 mg
- 236
- 209
- 181
- 26,400
- In stock
- 100 mg
- 418
- 371
- 321
- 46,800
- In stock
- 200 mg
- 633
- 562
- 487
- 70,800
- In stock
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- M.W. 309.33
- C15H15N7O
- [1224844-38-5]
- INK128 is a potent mTOR kinase inhibitor with a Ki of 1.4 nM. It had therapeutic benefit for prostate cancer metastasis. Hsieh A.C., et al. "The translational landscape of mTOR signalling steers cancer initiation and metastasis." Nature 485: 55-61 (2012).
- INK128 potently blocked cell proliferation in various breast cancer cell lines harboring PIK3CA (IC50 = 1.5-53 nM), PTEN (IC50 = 1-149 nM), KRAS and/or BRAF mutations (IC50 = 13-162 nM), and in human endothelial cells (IC50 = 33-40 nM) in vitro. In vivo, INK128 suppressed primary tumor growth significantly in both non-VEGF and VEGF-driven MCF-7 xenograft models. Gökmen-Polar Y., et al. "Investigational drug MLN0128, a novel TORC1/2 inhibitor, demonstrates potent oral antitumor activity in human breast cancer xenograft models." Breast Cancer Res. Treat. 136: 673-682 (2012).
- INK128 inhibited proliferation of B-cell acute lymphoblastic leukemia (B-ALL) cell lines in vitro and suppressed colony formation by primary human leukemia cells from adult and pediatric B-ALL patients. INK128 enhanced the efficacy of dasatinib in Philadelphia Chromosome-positive (Ph+) specimens. In a syngeneic mouse model of lymphoid BCR-ABL+ disease, INK128 rapidly cleared leukemic outgrowth. In non-Ph+, B-ALL xenografts, INK128 had a cytostatic effect. Janes M.R., et al. "Efficacy of the investigational mTOR kinase inhibitor MLN0128/INK128 in models of B-cell acute lymphoblastic leukemia." Leukemia 27: 586-594 (2013).
- The addition of lapatinib to INK-128 treatment resulted in inhibition of both PI3K/Akt/mTOR and ERK pathways and prevented both HER2 and HER3 phosphorylation induced by INK-128. This dual blockade demonstrated antitumor activity in preclinical models of breast cancer resistant to anti-HER2 therapy. García-García C., et al. "Dual mTORC1/2 and HER2 blockade results in antitumor activity in preclinical models of breast cancer resistant to anti-HER2 therapy." Clin. Cancer Res. 18: 2603-2612 (2012).
- Sold for laboratory or manufacturing purposes only; not for human, veterinary, food, or household use
- Not available in some countries; not available to some institutions; not available for some uses.
