BCATc Inhibitor 2

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BCATc Inhibitor 2

本产品不向个人销售，仅用作科学研究，不用于任何人体实验及非科研性质的动物实验。

CAS NO:

406191-34-2

包装与价格：

包装	价格(元)
5mg	电议
10mg	电议
50mg	电议

产品介绍

化学性质

Physical Appearance	A crystalline solid
Storage	Store at -20°C
M.Wt	418.8
Cas No.	406191-34-2
Formula	C₁₆H₁₀ClF₃N₂O₄S
Synonyms	Cytosolic Branched-Chain Amino Acid Transferase Inhibitor 2
Solubility	≤10mg/ml in ethanol;20mg/ml in DMSO;25mg/ml in dimethyl formamide
Chemical Name	5-chloro-2-benzofurancarboxylic acid 2-[[2-(trifluoromethyl)phenyl]sulfonyl]hydrazide
Canonical SMILES	ClC1=CC=C2C(C=C(C(NNS(C3=C(C(F)(F)F)C=CC=C3)(=O)=O)=O)O2)=C1
运输条件	蓝冰运输或根据您的需求运输。
一般建议	为了使其更好的溶解，请用37℃加热试管并在超声波水浴中震动片刻。不同厂家不同批次产品溶解度各有差异，仅做参考。若实验所需浓度过大至产品溶解极限，请添加助溶剂助溶或自行调整浓度。溶液形式一般不宜长期储存，请尽快用完。

资料参考

BCATc Inhibitor 2 is an active and selective inhibitor of cytosolic BCAT (BCATc)[1].

Branched-chain amino acid transferases (BCATs) have been implicated in catalyzing reversible transamination of isoleucine, leucine, and valine branched-chain amino acids to their corresponding α-keto acids, generating L-glutamate. It has been identified that there are two forms of BCAT in mammals: mitochondrial BCAT (BCATm) and cytosolic BCAT (BCATc). BCATc is expressed in particular brain region and involved in regulating glutamate synthesis for release during neuronal excitation. Thus, BCATc inhibition may be useful for the treatment of neurodegenerative and behavioral disorders involving disturbances of the glutamatergic system [2].

In vitro: BCATc inhibition is likely to be useful for the treatment of neurodegenerative and other neurological disorders involving disturbances of the glutamatergic system. In the hBCATc assays, BCATc Inhibitor 2 exhibited an IC50 of 0.8 ± 0.05 μM. In a recombinant rat BCATc assay and a crude rat BCATm assay, the IC50 was 0.2 μM ± 0.02 and 3.0 μM ± 0.5 (n=5), respectively. BCATc Inhibitor 2 decreased calcium influx in neuronal cultures with an IC50 of 4.8 ± 1.2 μM (n=4) [1].

In vivo: BCATc Inhibitor 2 blocked calcium influx into neuronal cells following inhibition of glutamate uptake, and demonstrated neuroprotective efficacy in vivo. In Lewis rats, after treatment with 30 mg/kg BCATc Inhibitor 2 (subcutaneous injection), the peak plasma concentration (Cmax) reached 8.28 μg/ml at 0.5 h (tmax). The mean plasma exposure (AUC) value was 19.9 μg h/ml, and the mean terminal half-life ranged from 12 to 15 h, indicating favorable PK parameters of BCATc Inhibitor 2. Daily administration of the mitochondrial neurotoxin, 3-nitroproprionic acid (3-NP) produced striatal lesions and led to motor deficits. Administration of BCATc Inhibitor 2 for 9 days almost completely reversed the effects of 3-NP [1].

References:
[1] Hu L Y, Boxer P A, Kesten S R, et al. The design and synthesis of human branched-chain amino acid aminotransferase inhibitors for treatment of neurodegenerative diseases[J]. Bioorganic & medicinal chemistry letters, 2006, 16(9): 2337-2340.
[2] Brosnan J T, Brosnan M E. Branched-chain amino acids: enzyme and substrate regulation[J]. The Journal of nutrition, 2006, 136(1): 207S-211S.

试验操作

Cell experiment:[1]
Cell lines	Neuronal cells
Reaction Conditions	4.8 μM BCATc Inhibitor 2 (IC50)
Applications	BCATc Inhibitor 2 blocked calcium influx into neuronal cells following inhibition of glutamate uptake, with an IC50 value of 4.8 ± 1.2 μM.
Animal experiment:[1]
Animal models	Lewis rats treated for 9 days with the 3-nitroproprionic acid (3-NP)
Dosage form	30 mg/kg/day Injected subcutaneously for 9 days
Applications	BCATc Inhibitor 2 (administered for 9 days) was able to almost completely reverse 3-NP-induced motor deficits, as evidenced by improved rotorod and beam walking performance. In addition, histological examination of the brains from these animals demonstrated significant reduction in the number of sections with degenerating neurons. Thus, BCATc inhibition may be useful for the treatment of neurodegenerative and behavioral disorders involving disturbances of the glutamatergic system.
Note	The technical data provided above is for reference only.
	References: 1. Hu LY, Boxer PA, Kesten SR, et al. The design and synthesis of human branched-chain amino acid aminotransferase inhibitors for treatment of neurodegenerative diseases. Bioorganic & Medicinal Chemistry Letters, 2006, 16(9): 2337-2340.