2 years -20°C Powder, 2 weeks 4°C in DMSO, 6 months -80°C in DMSO
Biological activity
Description
Target:
GI50: 13.48 nM (in K562 cells)[1].
In Vivo
TAI-1 (20 mg/kg intravenously IV/ or 150 mg/kg per oral PO/BID) inhibits tumor growth in multiple cancer xenograft models[1]. Animal Model: C.B-17 SCID mice (6-7 weeks, 21-24 g)[1]. Dosage: 20 mg/kg intravenously IV/ or 150 mg/kg per oral PO/BID. Administration: QDx28 cycles. Result: Led to significant tumor growth retardation in Huh-7 and modest tumor inhibition was noted tor the Colo205 and MDA-MB-231 models. Did not lead to any loss in body weight.
In Vitro
TAI-1 disrupts Hec1-Nek2 protein interaction, leads to Nek2 degradation, induces significant chromosomal misalignment in metaphase, and induces apoptotic cell death[1]. TAI-1 induces cancer cell death through the induction of cleavage of apoptotic proteins Caspase 3 and PARP and degradation of anti-apoptotic proteins MCL-1 and suggests that TAI-1 leads to activation of the apoptotic pathways[1]. TAI-1 is effective in many cancer cells, such as Chronic myeloid leukemia, Cervical cancer, Breast, metastatic-pleural, invasive ductal carcinoma, Acute myeloid leukemia, Myelogenous leukemia, Colorectal carcinoma cells, with GI50 less than 100 nM[1].
Kinase Assay
Cell Assay
Animal Administration
References
[1]. Lynn Y L Huang, et al. Characterization of the Biological Activity of a Potent Small Molecule Hec1 Inhibitor TAI-1. J Exp Clin Cancer Res. 2014 Jan 9;33(1):6.
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