2. Apoptosis
  3. RIP kinase
  4. RIPK1-IN-35

RIPK1-IN-35 是一种具有选择性和口服活性 RIPK1 抑制剂，其 IC50 为 5.33 nM。RIPK1-IN-35 对人和小鼠细胞的坏死性凋亡均具有显著的保护作用。RIPK1-IN-35 在 TNF-α 诱导的全身炎症反应综合征和 DSS (HY-116282C) 诱导的炎症性肠病模型中均显示出良好的治疗效果。RIPK1-IN-35 可用于研究与坏死性凋亡相关的炎症性疾病。

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RIPK1-IN-35

RIPK1-IN-35 Chemical Structure

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RIPK1-IN-35 相关抗体

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查看 RIP kinase 亚型特异性产品:

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RIPK1 RIPK2 RIPK3

  • 生物活性

  • 纯度 & 产品资料

  • 参考文献

生物活性

RIPK1-IN-35 is a selective and orally active RIPK1 inhibitor with an IC50 of 5.33 nM. RIPK1-IN-35 has a potent protective effect against necroptosis in both human and murine cells. RIPK1-IN-35 shows good therapeutic effects in both TNF-α-induced systemic inflammatory response syndrome and DSS (HY-116282C)-induced inflammatory bowel disease models. RIPK1-IN-35 can be used to the study of inflammatory diseases related to necroptosis[1].

产品应用

1. 该化合物可作为示踪剂。
2. 该化合物可作为 NMR、GC-MS 或 LC-MS 分析中的内标品，用于定量分析。
IC50 & Target[1]

RIPK1

5.33 nM (IC50)

体外研究
(In Vitro)

RIPK1-IN-35 (Compound 44) (0.01 nM-10 μM, 18 h) 可保护人源和鼠源细胞系免受 TSZ (TNF-α、BV6 (HY-16701) 和 Z-VAD-FMK (HY-16658B)) 诱导的坏死性凋亡，在 U937 和 L929 细胞中的 EC50 值分别为 18.1 nM 和 11.5 nM[1]。
RIPK1-IN-35 (0-300 nM, 5 h) 可显著且呈剂量依赖性地抑制 HT-29 细胞中 RIPK1 及其下游蛋白 RIPK3 和 MLKL 的磷酸化[1]。

MCE has not independently confirmed the accuracy of these methods. They are for reference only.

RIPK1-IN-35 相关抗体:

Western Blot Analysis[1]

Cell Line: HT-29 cells
Concentration: 0, 1, 3, 10, 30 and 100 nM
Incubation Time: Pretreated for 1 h and added TSZ for 4 h
Result: Significantly and dose-dependently inhibited the phosphorylation of RIPK1 as well as its downstream proteins RIPK3 and MLKL.
体内研究
(In Vivo)

RIPK1-IN-35 (Compound 44) (3-10 mg/kg，口服，单次给药) 能有效对抗 TNF-α 诱导的致命性全身炎症，并显著提高小鼠的存活率[1]。
RIPK1-IN-35 (10 mg/kg，口服，每日一次，连续 7 天) 在 DSS 诱导的炎症性肠病 (IBD) 模型中显示出显著的治疗效果，能有效缓解疾病的临床症状和病理损伤[1]。

MCE has not independently confirmed the accuracy of these methods. They are for reference only.

Animal Model: The model of systemic inflammatory response syndrome (SIRS) induced by TNF-α established in C57BL/6J mice (female, 6-8 weeks old)[1]
Dosage: 3 and 10 mg/kg
Administration: Oral administration (p.o.), single dose
Result: Dosage-dependently alleviated the sudden drop in body temperature caused by TNF-α.
Provided 80% and 100% survival protection rates respectively at doses of 3 mg/kg and 10 mg/kg.
Animal Model: DSS-induced IBD model established in C57BL/6J mice (female, 6-8 weeks old)[1]
Dosage: 10 mg/kg
Administration: Oral administration (p.o.), once daily for 7 days
Result: Significantly reduced the weight loss caused by DSS and improved the DAI score.
Significantly improved the phenomenon of colonic shortening.
Significantly alleviated severe epithelial damage, necrosis and infiltration of inflammatory cells, with a more intact mucosal structure and reduced inflammatory infiltration.
分子量

557.50

Formula

C26H18D3F3N6O5
运输条件

Room temperature in continental US; may vary elsewhere.
储存方式

Please store the product under the recommended conditions in the Certificate of Analysis.
纯度 & 产品资料
参考文献

RIPK1-IN-35 相关分类

  • 摩尔计算器

  • 稀释计算器

The molarity calculator equation

Mass (g) = Concentration (mol/L) × Volume (L) × Molecular Weight (g/mol)

质量   浓度   体积   分子量 *
= × ×

The dilution calculator equation

Concentration (start) × Volume (start) = Concentration (final) × Volume (final)

This equation is commonly abbreviated as: C1V1 = C2V2

浓度 (start) × 体积 (start) = 浓度 (final) × 体积 (final)
× = ×
C1   V1   C2   V2
Help & FAQs
  • Do most proteins show cross-species activity?

    Species cross-reactivity must be investigated individually for each product. Many human cytokines will produce a nice response in mouse cell lines, and many mouse proteins will show activity on human cells. Other proteins may have a lower specific activity when used in the opposite species.

Keywords:

RIPK1-IN-35RIP kinaseReceptor-interacting protein kinasesRIPKnecroptosisinflammatory diseasestructure-activity relationshippharmacokineticsin vivo efficacyTNF-α-induced SIRSDSS-induced IBDInhibitorinhibitorinhibit

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