| Company Name: |
BOC Sciences |
| Tel: |
16314854226 |
| Email: |
info@bocsci.com |
D-Tryptophan (2E)-2-(6-quinoxalinylmethylene)hydrazide manufacturers
- Rhosin
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- $1980.00
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2026-04-21
- CAS:1173671-63-0
- Purity:
- Supply Ability: 10g
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| | D-Tryptophan (2E)-2-(6-quinoxalinylmethylene)hydrazide Basic information |
| | D-Tryptophan (2E)-2-(6-quinoxalinylmethylene)hydrazide Chemical Properties |
| density | 1.38±0.1 g/cm3(Predicted) | | storage temp. | +2C to +8C | | solubility | Soluble in DMSO | | form | Orange brown powder | | pka | 12.00±0.46(Predicted) | | color | orange-brown |
| WGK Germany | WGK 3 | | Storage Class | 11 - Combustible Solids |
| | D-Tryptophan (2E)-2-(6-quinoxalinylmethylene)hydrazide Usage And Synthesis |
| Uses | Rho Inhibitor, Rhosin has been used to tre at single breast tumor cells to regulate RhoA activity to validate the cell line with the Frster resonance energy transfer (FRET) biosensor. | | Definition | ChEBI: Rhosin is a D-tryptophan derivative obtained by formal condensation of the carboxy group of D-tryptophan with the amino group of (quinoxalin-6-yl)methylidenehydrazide. It directly targets the Rho GEF binding domain, thereby preventing Rho from interacting with its GEFs It has a role as a RhoA inhibitor, a RhoC inhibitor and an antineoplastic agent. It is a D-tryptophan derivative, a quinoxaline derivative and a hydrazone. | | General Description | A cell-permeable (quinoxalinylmethylidene-D-tryptophanyl)hydrazide that directly targets Rho GEF binding domain (Kd = 354 nM for RhoA), thereby prevents Rho from interacting with its GEFs (including LARG, DBL, LBC, p115 RhoGEF, and PDZ RhoGEF), but not p190RhoGAP, RhoGDI, or its effectors (ROCK, mDia, PKN, Rhoteckin). Shown to suppress mammospheres formation in MCF7, but not the non-tumorigenic MCF10A, cultures and inhibit serum-induced RhoA, RhoB, and RhoC, but not Cdc42 or Rac1, activation, MLC & PAK phosphorylation, as well as stress fiber and focal complex formation in serum-starved NIH3T3 cultures (Effective conc. 30 μM) in a reversible manner. RhoA inactivation by G04 treatment (30 μM) is also demonstrated to promote neurite outgrowth and branching from NGF-treated PC12 cells. | | Biochem/physiol Actions | Primary TargetRho GTPase | | in vivo | Rhosin (40 mg/kg; i.p.) treatment prevents social avoidance caused by social defeat stress. Rhosin also blocks sucrose preference deficits induced by defeat in C57Bl6/J (Jackson) mice[1].
Rhosin (30 μM; bilateral, intra- Nucleus Accumbens (NAc) infusions) attenuates stress-induced social avoidance. Rhosin blocks stress-induced hyperexcitability in NAc dopamine 1 receptor medium spiny neurons (D1-MSNs). Rhosin prevents decreased excitatory transmission on NAc D1-MSNs. Rhosin enhances spine density in defeat mice[1]. | Animal Model: | D1-GFP or D2-GFP hemizygote mice on a C57BL/6J background[3] | | Dosage: | 40 mg/kg | | Administration: | i.p. | | Result: | Rhosin was systemically administered 15 min prior to defeat to block RhoA activation. While defeat significantly reduced the time that experimental mice spent interacting with a novel mouse, Rhosin administration suppressed this effect without affecting locomotor behaviors.
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| | D-Tryptophan (2E)-2-(6-quinoxalinylmethylene)hydrazide Preparation Products And Raw materials |
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