Home>>Signaling Pathways>> Others>> PDHK>>KPLH1130

KPLH1130 Sale

目录号 : GC36396

KPLH1130 is a specific inhibitor of pyruvate dehydrogenase kinase (PDK) that blocks macrophage polarization and attenuates proinflammatory responses.

KPLH1130 Chemical Structure

Cas No.:906669-07-6

规格 价格 库存 购买数量
10mM (in 1mL DMSO)
¥2,772.00
现货
1mg
¥855.00
现货
5mg
¥2,520.00
现货
10mg
¥4,050.00
现货
25mg
¥7,650.00
现货
50mg
¥11,700.00
现货
100mg
¥16,200.00
现货

电话:400-920-5774 Email: sales@glpbio.cn

Customer Reviews

Based on customer reviews.

Sample solution is provided at 25 µL, 10mM.

产品文档

Quality Control & SDS

View current batch:

产品描述

KPLH1130 is a specific inhibitor of pyruvate dehydrogenase kinase (PDK) that blocks macrophage polarization and attenuates proinflammatory responses.

[1] Min BK, et al. Front Immunol. 2019 May 7;10:944.

Chemical Properties

Cas No. 906669-07-6 SDF
Canonical SMILES OC1=CC=C(C2=NNC(N2C3=CC=C(C)C=C3)=O)C(O)=C1
分子式 C15H13N3O3 分子量 283.28
溶解度 DMSO: 135 mg/mL (476.56 mM) 储存条件 Store at -20°C
General tips 请根据产品在不同溶剂中的溶解度选择合适的溶剂配制储备液;一旦配成溶液,请分装保存,避免反复冻融造成的产品失效。
储备液的保存方式和期限:-80°C 储存时,请在 6 个月内使用,-20°C 储存时,请在 1 个月内使用。
为了提高溶解度,请将管子加热至37℃,然后在超声波浴中震荡一段时间。
Shipping Condition 评估样品解决方案:配备蓝冰进行发货。所有其他可用尺寸:配备RT,或根据请求配备蓝冰。

溶解性数据

制备储备液
1 mg 5 mg 10 mg
1 mM 3.5301 mL 17.6504 mL 35.3008 mL
5 mM 0.706 mL 3.5301 mL 7.0602 mL
10 mM 0.353 mL 1.765 mL 3.5301 mL
  • 摩尔浓度计算器

  • 稀释计算器

  • 分子量计算器

质量
=
浓度
x
体积
x
分子量
 
 
 
*在配置溶液时,请务必参考产品标签上、MSDS / COA(可在Glpbio的产品页面获得)批次特异的分子量使用本工具。

计算

动物体内配方计算器 (澄清溶液)

第一步:请输入基本实验信息(考虑到实验过程中的损耗,建议多配一只动物的药量)
给药剂量 mg/kg 动物平均体重 g 每只动物给药体积 ul 动物数量
第二步:请输入动物体内配方组成(配方适用于不溶于水的药物;不同批次药物配方比例不同,请联系GLPBIO为您提供正确的澄清溶液配方)
% DMSO % % Tween 80 % saline
计算重置

Research Update

Pyruvate Dehydrogenase Kinase Is a Metabolic Checkpoint for Polarization of Macrophages to the M1 Phenotype

Front Immunol 2019 May 7;10:944.PMID:31134063DOI:PMC6514528

Metabolic reprogramming during macrophage polarization supports the effector functions of these cells in health and disease. Here, we demonstrate that pyruvate dehydrogenase kinase (PDK), which inhibits the pyruvate dehydrogenase-mediated conversion of cytosolic pyruvate to mitochondrial acetyl-CoA, functions as a metabolic checkpoint in M1 macrophages. Polarization was not prevented by PDK2 or PDK4 deletion but was fully prevented by the combined deletion of PDK2 and PDK4; this lack of polarization was correlated with improved mitochondrial respiration and rewiring of metabolic breaks that are characterized by increased glycolytic intermediates and reduced metabolites in the TCA cycle. Genetic deletion or pharmacological inhibition of PDK2/4 prevents polarization of macrophages to the M1 phenotype in response to inflammatory stimuli (lipopolysaccharide plus IFN-γ). Transplantation of PDK2/4-deficient bone marrow into irradiated wild-type mice to produce mice with PDK2/4-deficient myeloid cells prevented M1 polarization, reduced obesity-associated insulin resistance, and ameliorated adipose tissue inflammation. A novel, pharmacological PDK inhibitor, KPLH1130, improved high-fat diet-induced insulin resistance; this was correlated with a reduction in the levels of pro-inflammatory markers and improved mitochondrial function. These studies identify PDK2/4 as a metabolic checkpoint for M1 phenotype polarization of macrophages, which could potentially be exploited as a novel therapeutic target for obesity-associated metabolic disorders and other inflammatory conditions.