Dayang Chem (Hangzhou) Co., Ltd.
China
Product Name: 4-Chloro-N-(naphthalen-1-ylmethyl)-5-(3-(piperazin-1-yl)phenoxy)thiophene-2-sulfonamide
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Purity: 98.0%
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1261576-81-1

1261576-81-1 structure

Name: B355252
Chemical Name: 4-Chloro-N-(1-naphthylmethyl)-5-[3-(1-piperazinyl)phenoxy]-2-thiophenesulfonamide
CAS Number: 1261576-81-1
Molecular Formula: C₂₅H₂₄ClN₃O₃S₂
Molecular Weight: 514.059
Create Date: 2018-06-29 04:21:08
Modify Date: 2025-08-21 13:51:03
B355252, a phenoxy thiophene sulfonamide small molecule, is a potent NGF receptor agonist. B355252 potentiates NGF-induced neurite outgrowth. B355252 protects ischemic neurons from neuronal loss by attenuating DNA damage, reducing ROS production and the LDH level, and preventing neuronal apoptosis. B355252 has anti-apoptotic effects in glutamate-induced excitotoxicity, as well as in a murine hippocampal cell line (HT22) model of Parkinson disease (PD)[1].

Name	4-Chloro-N-(1-naphthylmethyl)-5-[3-(1-piperazinyl)phenoxy]-2-thiophenesulfonamide
Synonyms	2-Thiophenesulfonamide, 4-chloro-N-(1-naphthalenylmethyl)-5-[3-(1-piperazinyl)phenoxy]- 4-Chloro-N-(1-naphthylmethyl)-5-[3-(1-piperazinyl)phenoxy]-2-thiophenesulfonamide MFCD28100813

Description	B355252, a phenoxy thiophene sulfonamide small molecule, is a potent NGF receptor agonist. B355252 potentiates NGF-induced neurite outgrowth. B355252 protects ischemic neurons from neuronal loss by attenuating DNA damage, reducing ROS production and the LDH level, and preventing neuronal apoptosis. B355252 has anti-apoptotic effects in glutamate-induced excitotoxicity, as well as in a murine hippocampal cell line (HT22) model of Parkinson disease (PD)[1].
Related Catalog	Signaling Pathways >> Apoptosis >> Apoptosis Research Areas >> Neurological Disease
In Vivo	B-355252 (0.125 mg/kg; ip; daily; 3 days) significantly attenuates the infarct volume and protects post-stroke neuronal loss in adult male Sprague–Dawley rats with cerebral ischemia[1].
References	[1]. Hao-Kuang Wang, et al. A Novel NGF Receptor Agonist B355252 Ameliorates Neuronal Loss and Inflammatory Responses in a Rat Model of Cerebral Ischemia. J Inflamm Res. 2021 Jun 1;14:2363-2376.