Tuesday 27 September 2022 - 03:53
In Business 42 Years - Since 1980
Recently, we have been and are currently operating with: (1) staff shortages related to CV19 and other factors, (2) vacations, (3) a significant health burden for one senior staff member, and (4) dedication of substantial internal resources to a major public-service project. This situation is expected to continue through Sunday, September 11. During this time, we have been and expect to continue entering, processing and shipping orders normally for in-stock products. However, non-order-related communications and production of backordered products will be subject to some unusual delays. We apologize very much for this situation and appreciate your understanding.
FREE SHIPPING TO THE U.S. AND 32 OTHER COUNTRIES! [Read more].
I-3344 INK128, Free Base, >99%
Synonyms : [MLN0128] [Sapanisertib]
- Size
- US $
- €
- £
- ¥
- 25 mg
- 155
- 160
- 143
- 22,400
- In stock
- 50 mg
- 236
- 244
- 218
- 34,100
- In stock
- 100 mg
- 418
- 433
- 387
- 60,300
- In stock
- 200 mg
- 633
- 656
- 586
- 91,300
- In stock
- 300 mg
- 864
- 895
- 800
- 124,700
- In stock
- 500 mg
- 1,245
- 1,291
- 1,152
- 179,600
- In stock
- 1 g
- 1,930
- 2,001
- 1,787
- 278,500
- In stock
Note: Our Euro, Pound, and Yen prices are revised regularly to account for currency exchange rate fluctuations.
- 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.
