BTSA1

Modify Date: 2024-02-01 06:23:17

BTSA1 Structure
BTSA1 structure
Common Name BTSA1
CAS Number 314761-14-3 Molecular Weight 430.505
Density 1.5±0.1 g/cm3 Boiling Point 625.2±48.0 °C at 760 mmHg
Molecular Formula C21H14N6OS2 Melting Point N/A
MSDS N/A Flash Point 331.9±29.6 °C

 Use of BTSA1


BTSA1 is a potent, high affinity and orally active BAX activator with an IC50 of 250 nM and an EC50 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[1].

 Names

Name BTSA1
Synonym More Synonyms

 BTSA1 Biological Activity

Description BTSA1 is a potent, high affinity and orally active BAX activator with an IC50 of 250 nM and an EC50 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[1].
Related Catalog
Target

Bax:250 nM (IC50)

Bax:144 nM (EC50)

In Vitro 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[1]. 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[1]. 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[1]. Cell Viability Assaysup>[1] Cell Line: Human AML cell lines< Concentration: 5 μM Incubation Time: 6 hours, 12 hours, 24 hours Result: Reduced viability of all AML cell lines. Displayed substantial cell death activity within 6 hours. Western Blot Analysis[1] Cell Line: NB4 cells Concentration: 2.5 μM, 5 μM, 10 μM Incubation Time: 6 hours Result: Significant BAX mitochondrial translocation was induced in a dose-dependent manner. Apoptosis Analysis[1] Cell Line: OCI-AML3 cells Concentration: 0.15625 μM, 0.3125 μM, 0.625 μM, 1.25 μM, 2.5 μM, 5 μM, 10 μM Incubation Time: 4 hours, 6 hours, 8 hours, 12 hours, 24 hours Result: Induced dose-dependent caspase-3/7 activation in OCI-AML3 cells. Caspase-3/7 activation was monitored within 4-24 hr and maximal caspase-3/7 activation was detected in 4 hr.
In Vivo 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[1]. Animal Model: NOD-SCID IL2Rγ null (NSG) mice (6-8 weeks old) with THP-1 cells[1] Dosage: 10 mg/kg Administration: Intraperitoneal injection; every two days Result: Significantly increased survival when compared to vehicle-treated mice.
References

[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.

 Chemical & Physical Properties

Density 1.5±0.1 g/cm3
Boiling Point 625.2±48.0 °C at 760 mmHg
Molecular Formula C21H14N6OS2
Molecular Weight 430.505
Flash Point 331.9±29.6 °C
Exact Mass 430.067047
LogP 3.68
Vapour Pressure 0.0±1.8 mmHg at 25°C
Index of Refraction 1.791
Storage condition -20℃

 Synonyms

(4Z)-5-Phenyl-2-(4-phenyl-1,3-thiazol-2-yl)-4-(1,3-thiazol-2-ylhydrazono)-2,4-dihydro-3H-pyrazol-3-one
1H-Pyrazole-4,5-dione, 3-phenyl-1-(4-phenyl-2-thiazolyl)-, 4-[2-(2-thiazolyl)hydrazone], (4Z)-
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