BTSA1 是一种有效的，高亲和力和口服活性的 BAX 激活剂，IC₅₀ 为 250 nM，EC₅₀ 为 144 nM。BTSA1 以高亲和力和特异性与 N 末端激活位点结合，并诱导 BAX 发生构象变化，从而导致 BAX 介导的细胞凋亡。

BTSA1 is a potent, high affinity and orally active BAX activator with an IC 50 of 250 nM and an EC 50 of 144 nM. BTSA1 binds with high affinity and specificity to the N-terminal activation site and induces conformational changes to BAX leading to BAX-mediated apoptosis.

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Bax 250 nM (IC50) Bax 144 nM (EC50

BTSA1 (5 μM; 6-24 hours; human AML cell lines) treatment reduced viability of all AML cell lines and displays substantial cell death activity within 6 hours.
BTSA1 (2.5-10 μM; 6 hours; NB4 cells) treatment induces BAX translocation coincided with the release of cytochrome c from the mitochondria to the cytosol. Significant BAX mitochondrial translocation is induced in a BTSA1 dose-dependent manner.
BTSA1 (0.15625-10 μM; 4-24 hours; OCI-AML3 cells) treatment induces dose-dependent caspase-3/7 activation in OCI-AML3 cells. Caspase-3/7 activation is monitored within 4-24 hours and maximal caspase-3/7 activation is detected in 4 hours. has not independently confirmed the accuracy of these methods. They are for reference only.

BTSA1 (10 mg/kg; intraperitoneal injection; every two days; NOD-SCID IL2Rγ null (NSG) mice) treatment significantly increases survival when compared to vehicle-treated mice. BTSA1 treatment induces significant suppression of leukemia growth. has not independently confirmed the accuracy of these methods. They are for reference only.

Room temperature in continental US; may vary elsewhere.

Powder -20°C 3 years；4°C 2 years

[1]. Reyna DE, et al. Direct Activation of BAX by BTSA1 Overcomes Apoptosis Resistance in Acute Myeloid Leukemia. Cancer Cell. 2017 Oct 9;32(4):490-505.e10.

In Vitro: DMSO : 25 mg/mL (58.07 mM; Need ultrasonic)配制储备液