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NVS-PI3-4 Sale

目录号 : GC62141

NVS-PI3-4 是一种特异性 PI3Kγ 抑制剂。 NVS-PI3-4 可用于过敏,炎症和癌症疾病的研究。

NVS-PI3-4 Chemical Structure

Cas No.:941580-60-5

规格 价格 库存 购买数量
5 mg
¥2,250.00
现货
10 mg
¥3,600.00
现货
25 mg
¥7,650.00
现货

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Sample solution is provided at 25 µL, 10mM.

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产品描述

NVS-PI3-4 is a specific PI3Kγ inhibitor. NVS-PI3-4 can be used for the research of allergies, inflammatory and cancer diseases[1][2].

NVS-PI3-4 shows an exquisite cellular selectivity for PI3Kγ. NVS-PI3-4 reduces IgE/antigen-mediated phosphorylation of PKB/Akt in p110δDA. NVS-PI3-4 (5 μM; 30 minutes; BMMCs) is not accumulate in specifically in mast cells[2].

[1]. Bruce I, et al. Development of isoform selective PI3-kinase inhibitors as pharmacological tools for elucidating the PI3K pathway. Bioorg Med Chem Lett. 2012;22(17):5445-5450.
[2]. Collmann E, et al. Transient targeting of phosphoinositide 3-kinase acts as a roadblock in mast cells’ route to allergy. J Allergy Clin Immunol. 2013;132(4):959-968.

Chemical Properties

Cas No. 941580-60-5 SDF
分子式 C20H26N4O3S 分子量 402.51
溶解度 DMSO : 250 mg/mL (621.10 mM; Need ultrasonic) 储存条件 Store at -20°C
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1 mg 5 mg 10 mg
1 mM 2.4844 mL 12.4221 mL 24.8441 mL
5 mM 0.4969 mL 2.4844 mL 4.9688 mL
10 mM 0.2484 mL 1.2422 mL 2.4844 mL
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Research Update

Transient targeting of phosphoinositide 3-kinase acts as a roadblock in mast cells' route to allergy

J Allergy Clin Immunol 2013 Oct;132(4):959-68.PMID:23683463DOI:10.1016/j.jaci.2013.03.008

Background: Tissue mast cell numbers are dynamically regulated by recruitment of progenitors from the vasculature. It is unclear whether progenitors are recruited during allergic sensitization and whether recruitment promotes allergic responses. Objective: We sought to (1) determine the effect of mast cell recruitment on acute allergic responses and (2) to define the role of phosphoinositide 3-kinase (PI3K) isoforms in sequential steps to allergic responses. Methods: Gene-targeted mice for PI3Kγ or PI3Kδ or mice treated with isoform-specific PI3K inhibitors (a novel PI3Kγ-specific inhibitor [NVS-PI3-4] and the PI3Kδ inhibitor IC87114) were used to monitor IgE-mediated mast cell recruitment, migration, adhesion by means of intravital microscopy, degranulation, TNF-α release, and subsequent endothelial cell activation in vivo or in bone marrow-derived mast cells. Results: Functional PI3Kγ, but not PI3Kδ, was crucial for mast cell accumulation in IgE-challenged skin, TNF-α release from IgE/antigen-stimulated mast cells, and mast cell/endothelial interactions and chemotaxis. PI3Kγ-deficient bone marrow-derived mast cells did not adhere to the endothelium in TNF-α-treated cremaster muscle, whereas PI3Kδ was not required. Depletion of TNF-α blocked IgE-induced mast cell recruitment, which links tissue mast cell-derived cytokine release to endothelial activation and mast cell recruitment. Interference with mast cell recruitment protected against anaphylaxis and was superior to blockage of tissue mast cell degranulation. Conclusions: Interference with mast cell recruitment to exacerbated tissues provides a novel strategy to alleviate allergic reactions and surpassed attenuation of tissue mast cell degranulation. This results in prolonged drug action and allows for reduction of drug doses required to block anaphylaxis, an important feature for drugs targeting inflammatory disease in general.