GW3965 HCl|2mg|K1327-上海高创化学科技有限公司

GW3965 HCl

参考价：¥660

供货周期：

一周

品牌：

规格：

2mg

货号：

K1327

CAS号：

405911-17-3

SKU:K1327		M. Wt:618.51
Formula:C33H31ClF3NO3.HCl		Solubility:No
Purity:>99%		Storage:2 years at -20 degrees centigrade
CAS No.:405911-17-3		Synonyms:N/A
Chemical NameN/A

Description	GW3965 HCl
Targets	LXRalpha/SRC1?LiSA	LXRalpha-GAL4
IC50	125 nM(EC50)	190 nM(EC50)
In vitro	GW3965 can inhibit liver X receptor (LXR), which can activate genes that regulate lipid and cholesterol metabolism. Treatment of primary human hepatocytes with GW3965 results in reduced output of bile acids and very low density lipoprotein triglycerides and induced expression of adipose differentiation-related protein accompanied by increased lipid storage. In pentobarbital-anesthetized male Sprague-Dawley rats, after oral administration of GW3965 (10 mg kg(-1), q.d.) , GW3965 dosing blunted the vasopressor effect of Ang II, which was significantly different with the 0.3 and 3 microg kg(-1) doses. GW3965 decreased Ang II-mediated vasopressor responses coincident with a trend toward reduced ATR gene expression, suggesting that LXR agonists could affect vascular reactivity. GW3965 could modulate the inflammatory status of human pancreatic islets. Treatment of LPS-stimulated human islets with the synthetic LXR agonist GW3965 (1 micromol/l) for 24 h reduced mRNA and protein levels of selected pro-inflammatory cytokines (IL-8, monocyte chemotactic protein-1 and tissue factor). Even liver X receptor (LXR) agonism has previously been shown to increase insulin release from pancreatic islets and reduce inflammation in leucocytes, GW3965,as a agonist of agonist, had no adverse effect on insulin secretion, islet viability or apoptosis.
In vivo	GW3965 can induce transcription of several genes including ABCA1 and apoE, and reduce Abeta levels and improve cognition in AD mice. Treatment of APP/PS1 mice with GW3965 increased ABCA1 and apoE protein levels.At 33 mg/kg/day, GW3965 was also associated with a trend toward redistribution of Abeta to the carbonate-soluble pool independent of ABCA1.
Clinical Trials	N/A
Features	N/A

Description

GW3965 HCl

Targets

LXRalpha/SRC1?LiSA

LXRalpha-GAL4

IC50

125 nM(EC50)

190 nM(EC50)

In vitro

GW3965 can inhibit liver X receptor (LXR), which can activate genes that regulate lipid and cholesterol metabolism. Treatment of primary human hepatocytes with GW3965 results in reduced output of bile acids and very low density lipoprotein triglycerides and induced expression of adipose differentiation-related protein accompanied by increased lipid storage. In pentobarbital-anesthetized male Sprague-Dawley rats, after oral administration of GW3965 (10 mg kg(-1), q.d.) , GW3965 dosing blunted the vasopressor effect of Ang II, which was significantly different with the 0.3 and 3 microg kg(-1) doses. GW3965 decreased Ang II-mediated vasopressor responses coincident with a trend toward reduced ATR gene expression, suggesting that LXR agonists could affect vascular reactivity. GW3965 could modulate the inflammatory status of human pancreatic islets. Treatment of LPS-stimulated human islets with the synthetic LXR agonist GW3965 (1 micromol/l) for 24 h reduced mRNA and protein levels of selected pro-inflammatory cytokines (IL-8, monocyte chemotactic protein-1 and tissue factor). Even liver X receptor (LXR) agonism has previously been shown to increase insulin release from pancreatic islets and reduce inflammation in leucocytes, GW3965,as a agonist of agonist, had no adverse effect on insulin secretion, islet viability or apoptosis.

In vivo

GW3965 can induce transcription of several genes including ABCA1 and apoE, and reduce Abeta levels and improve cognition in AD mice. Treatment of APP/PS1 mice with GW3965 increased ABCA1 and apoE protein levels.At 33 mg/kg/day, GW3965 was also associated with a trend toward redistribution of Abeta to the carbonate-soluble pool independent of ABCA1.

Clinical Trials

N/A

Features

N/A