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Merck
CN
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文件

安全信息

SML3706

Sigma-Aldrich

BT2

≥98% (HPLC)

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别名:
3,6-Dichloro-1-benzothiophene-2-carboxylic acid, 3,6-Dichlorobenzo[b]thiophene-2-carboxylic acid, 3,6-Dichlorobenzothiophene-2-carboxylic acid
经验公式（希尔记法）:
C9H4Cl2O2S
CAS号:
34576-94-8
分子量:
247.10
MDL编号:
MFCD00781745
UNSPSC代码:
12352200
NACRES:
NA.77

质量水平

100

检测方案

≥98% (HPLC)

形式

powder

颜色

white to beige

溶解性

DMSO: 2 mg/mL, clear

储存温度

2-8°C

生化/生理作用

BT2 is an orally active, allosteric mitochondrial branched-chain α-ketoacid dehydrogenase (BCKD) kinase (BCKDK or BDK) inhibitor (IC50 = 3.19 μM) that induces BDK dissociation from the BCKD complex (BCKDC) with superior pharmacokinetics and metabolic stability than (S)-CPP. BT2 increases cellular BCKDC activity in cultures (40 μM; MEF & murine hepatocytes) and induces BDK degradation in mice & rats in vivo, effectively upregulating tissue BCKDC activity and downregulating plasma branched-chain amino acid (BCAA) level. Typical dosing range: 40-250 μM (in cultures or cell-free), 20-40 mg/kg (ip. or po. in vivo; mice & rats) or 200 mg/kg diet.

WGK

WGK 3

闪点(°F)

Not applicable

闪点(°C)

Not applicable

法规信息

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Mengping Chen et al.
Journal of the American Heart Association, 8(11), e011625-e011625 (2019-08-23)
Background Branched-chain amino acid (BCAA) catabolic defect is an emerging metabolic hallmark in failing hearts in human and animal models. The therapeutic impact of targeting BCAA catabolic flux under pathological conditions remains understudied. Methods and Results BT2 (3,6-dichlorobenzo[b]thiophene-2-carboxylic acid), a
Golam M Uddin et al.
Cardiovascular diabetology, 18(1), 86-86 (2019-07-07)
Branched chain amino acids (BCAA) can impair insulin signaling, and cardiac insulin resistance can occur in the failing heart. We, therefore, determined if cardiac BCAA accumulation occurs in patients with dilated cardiomyopathy (DCM), due to an impaired catabolism of BCAA
Danielle Murashige et al.
Cell metabolism, 34(11), 1749-1764 (2022-10-13)
Pharmacologic activation of branched-chain amino acid (BCAA) catabolism is protective in models of heart failure (HF). How protection occurs remains unclear, although a causative block in cardiac BCAA oxidation is widely assumed. Here, we use in vivo isotope infusions to show

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