NSC-23766 trihydrochloride
NSC 23766
CAS: 1177865-17-6
Molecular Formula: C24H35N7
NSC-23766 trihydrochloride - Names and Identifiers
NSC-23766 trihydrochloride - Physico-chemical Properties
| Molecular Formula | C24H35N7 |
| Molar Mass | 421.5816 |
| Melting Point | >225°C (dec.) |
| Solubility | H2O: soluble10mg/mL, clear |
| Appearance | powder |
| Color | white to beige |
| Storage Condition | -20°C |
| In vitro study | NSC23766 is believed to fit into the surface grooves of Rac1, which is essential for GEF specifications. NSC23766 effectively inhibits Rac1 binding and activation by Rac-specific GEF Trio or Tiam1, in a dose-dependent manner, through its respective GEFs, does not interfere with the binding or activation of closely related Cdc42 or RhoA. NSC23766 effectively regulates Rac GTPase function in the cytoskeleton, and many cellular functions, including cell cycle, cell growth, adhesion, migration, and gene transcription. NSC 23766 (50 μm) effectively inhibited serum or platelet-derived growth factor-induced Rac1 activation and pseudopodia formation in NIH 3T3 cells without affecting endogenous Cdc42 or RhoA activity. NSC23766 reduces Trio or tim1 but not Vav, Lbc, Intersectin, and constitutively activated Rac1 mutant-stimulated NIH 3T3 cell growth and also inhibits Trio, tim1, or Ras-induced cell transformation. NSC23766 inhibited PC-3 of cell proliferation and Anchorage-independent growth in a dose-dependent manner. 25 μm NSC23766 inhibited cell invasion across the basement membrane by 85% PC-3. 50 μm NSC 23766 acts on human platelets, inhibiting thrombin-induced activation of Rac1 and Rac2, and platelet aggregation. NSC23766 inhibited Aβ40 and Aβ42 production in swAPP-HEK293 cells and did not affect Notch and soppα. NSC23766 inhibits gamma-secretase activity in cells, but not as a direct gamma-secretase inhibitor. NSC23766 reduced secreted and intracellular Aβ40 levels with an IC50 of 48.94 μm in a dose-dependent manner. 50 μm NSC 23766 inhibited 57.97% of Aβ42 release. NSC23766 regulates endothelial NO synthase expression and endothelial function. 100 μm NSC23766 inhibits eNOS promoter activity, 60% in bovine aortic endothelial cells, and 30% to 35% in bEND.3 cells. NSC23766 inhibits Rac1, disrupts eNOS mRNA stability, and shortens the half-life to 17 hours. NSC23766 inhibited ACh-induced aortic ring relaxation in wild-type mice in a dose-dependent manner. NSC23766 inhibits cell growth and induces apoptosis. NSC23766 reduced cell viability by MDA-MB-468 and MDA-MB-231 in a dose-dependent manner with an IC50 of ~ 10 μm, compared with estrogen receptor (ER), progesterone receptor (PR),Her2, and p53 gene mutation status. NSC23766 had little effect on the survival of MCF12A normal mammary epithelial cells. After 24 hours of NSC 23766 treatment of MDA-MB-231 cells, the G1 phase cells increased by 41% to 65%, and the S and G2-M phases decreased. 100 NSC23766 M induced MDA-MB-468 cell apoptosis increased 6 times. NSC23766 acts on breast cancer cells and inhibits cell cycle arrest or apoptosis by down-regulating cyclin D1, survivin, X-linked protein inhibitor of apoptosis (XIAP). |
| In vivo study | NSC23766 induces hematopoietic stem/precursor cell mobilization. Intraperitoneal injection of NSC23766 at a dose of 2.5 mg/kg into a poorly driven C57Bl/6 mouse strain resulted in a 2-fold enhancement of circulating hematopoietic stem/precursor cells 6 hours after injection. Mice treated with NSC23766 reduced lipopolysaccharide-induced acute by lung injury. NSC23766 at a dose of 1 or 3 mg/kg, not only reduces inflammatory cell infiltration and MPO activity, but also inhibits pro-inflammatory mediators, and tumor necrosis factor-alpha, interleukin-1 beta, mRNA expression. NSC23766 also reduced the accumulation of Evans Blue and albumin in LPS-treated lungs. |
NSC-23766 trihydrochloride - Risk and Safety
| Hazard Symbols | Xi - Irritant |
| Risk Codes | 36/37/38 - Irritating to eyes, respiratory system and skin. |
| Safety Description | 26 - In case of contact with eyes, rinse immediately with plenty of water and seek medical advice. |
| WGK Germany | 3 |
NSC-23766 trihydrochloride - Preparation solution concentration reference
| 1mg | 5mg | 10mg | |
|---|---|---|---|
| 1 mM | 1.883 ml | 9.417 ml | 18.834 ml |
| 5 mM | 0.377 ml | 1.883 ml | 3.767 ml |
| 10 mM | 0.188 ml | 0.942 ml | 1.883 ml |
| 5 mM | 0.038 ml | 0.188 ml | 0.377 ml |
Last Update：2024-01-02 23:10:35
NSC-23766 trihydrochloride - Reference Information
| biological activity | NSC 23766 is a RacGTPase inhibitor that activates Rac through guanine nucleotide exchange factors (GEFs), and IC50 is 50 μM; Does not inhibit closely related targets Cdc42 and RhoA. |
| in vitro studies | NSC23766 are considered to be able to blend into the surface grooves of Rac1, which is crucial to GEF specifications. NSC23766, through Rac-specific GEF Trio or Tiam1, effectively inhibit Rac1 binding and activation. This effect is dose-dependent and does not interfere with closely related Cdc42 or RhoA binding or activation through their respective GEFs. NSC23766 effectively regulate Rac GTPase function in cytoskeleton and many cell functions, including cell cycle, cell growth, adhesion, migration and gene transcription. NSC 23766 (50 μM) acts on NIH 3T3 cells, effectively inhibiting Rac1 activation and pseudopodia formation induced by serum or platelet-derived growth factors, and does not affect endogenous Cdc42 or RhoA activity. NSC23766 reduce the growth of NIH 3T3 cells stimulated by Trio or Tiam1 instead of Vav, Lbc, Intersectin, and constitutively activated Rac1 mutant, and also inhibit the cell transformation induced by Trio, Tiam1, or Ras. NSC23766 inhibit PC-3 cell proliferation and anchorage-independent growth, this effect is dose-dependent. 25 μM NSC23766 inhibited 85% PC-3 cell invasion across the basement membrane. 50 μM NSC 23766 acts on human platelets, inhibiting thrombin-induced Rac1 and Rac2 activation and platelet aggregation. NSC23766 acts on swAPP-HEK293 cells, inhibits the production of Aβ40 and Aβ42, and does not affect Notch and sAPP α. NSC23766 inhibits γ-secretase activity in cells, but not as a direct γ-secretase inhibitor. NSC23766 reduce secreted and intracellular Aβ40 levels, IC50 is 48.94 μM, which is dose-dependent. 50 μM NSC 23766 inhibited the release of 57.97% Aβ42. NSC23766 regulates endothelial NO synthase expression and endothelial function. 100 μM NSC23766 Inhibits eNOS Promoter Activity, 60% Inhibition in Bovine Aortic Endothelial Cells, bEND. Inhibition of 30% to 35% in 3 cells. NSC23766 inhibit Rac1, destroy the stability of eNOS mRNA, and shorten the half-life to 17 hours. NSC23766 inhibited ACh-induced relaxation of wild-type mouse aortic rings in a dose-dependent manner. NSC23766 inhibits cell growth and induces cell apoptosis. NSC23766 reduce MDA-MB-468 and MDA-MB-231 cell viability, this effect is dose-dependent, IC50 is ~ 10 μM, and has nothing to do with estrogen receptor (ER), progesterone receptor (PR),Her2, and p53 gene mutation status. NSC23766 had little effect on the survival of MCF12A normal mammary epithelial cells. After NSC 23766 treated MDA-MB-231 cells for 24 hours, G1 phase cells increased 41% to 65%, and S and G2-M phases decreased. 100 μM NSC23766 induced apoptosis of MDA-MB-468 cells to increase 6 times. NSC23766 acts on breast cancer cells, inhibits cell cycle arrest or apoptosis, and is regulated by down-regulating cyclin D1, survivin, X-linked protein apoptosis inhibitor (XIAP). |
| in vivo studies | NSC23766 induce hematopoietic stem cell/precursor cell mobilization. NSC23766 was injected intraperitoneally at a dose of 2.5 mg/kg into a poorly driven C57Bl/6 mouse strain. After 6 hours of injection, the circulating hematopoietic stem cells/precursor cells were 2-fold enhanced. Mice were NSC23766 treated to reduce acute lung injury induced by lipopolysaccharide. NSC23766 treated at a dose of 1 or 3 mg/kg not only reduced inflammatory cell infiltration and MPO activity, but also inhibited pro-inflammatory mediators, and tumor necrosis factor-α, interleukin-1β, and mRNA expression. NSC23766 also reduced Evans Blue and albumin accumulation in LPS-treated lungs. |
Last Update：2024-04-10 22:29:15
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Product Name: NSC 23766 Visit Supplier Webpage Request for quotationCAS: 1177865-17-6
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Email: 3008007409@qq.com
Mobile: 18021002903
QQ: 3008007409
Wechat: 18301782025
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