1. Signaling Pathways
  2. Apoptosis
  3. TNF Receptor

TNF Receptor (肿瘤坏死因子)

Tumor necrosis factor (TNF) is a major mediator of apoptosis as well as inflammation and immunity, and it has been implicated in the pathogenesis of a wide spectrum of human diseases, including sepsis, diabetes, cancer, osteoporosis, multiple sclerosis, rheumatoid arthritis, and inflammatory bowel diseases.

TNF-α is a 17-kDa protein consisting of 157 amino acids that is a homotrimer in solution. In humans, the gene is mapped to chromosome 6. Its bioactivity is mainly regulated by soluble TNF-α–binding receptors. TNF-α is mainly produced by activated macrophages, T lymphocytes, and natural killer cells. Lower expression is known for a variety of other cells, including fibroblasts, smooth muscle cells, and tumor cells. In cells, TNF-α is synthesized as pro-TNF (26 kDa), which is membrane-bound and is released upon cleavage of its pro domain by TNF-converting enzyme (TACE).

Many of the TNF-induced cellular responses are mediated by either one of the two TNF receptors, TNF-R1 and TNF-R2, both of which belong to the TNF receptor super-family. In response to TNF treatment, the transcription factor NF-κB and MAP kinases, including ERK, p38 and JNK, are activated in most types of cells and, in some cases, apoptosis or necrosis could also be induced. However, induction of apoptosis or necrosis is mainly achieved through TNFR1, which is also known as a death receptor. Activation of the NF-κB and MAPKs plays an important role in the induction of many cytokines and immune-regulatory proteins and is pivotal for many inflammatory responses.

目录号 产品名 作用方式 纯度
  • HY-11109
    Resatorvid Inhibitor 99.95%
    Resatorvid (TAK-242) 是一种选择性的 TLR4 信号传导抑制剂。Resatorvid 抑制 NOTNF-αIL-6 的产生,其 IC50 值分别为 1.8 nM,1.9 nM,1.3 nM。Resatorvid 下调 TLR4 下游信号分子 MyD88 和 TRIF 的表达。Resatorvid 抑制自噬 (autophagy),并在各种炎症性疾病中起关键作用。
  • HY-N0822
    Shikonin Inhibitor 99.80%
    Shikonin 是中草药紫草的主要成分。Shikonin 是一种有效的 TMEM16A 氯化物通道 (chloride channel) 抑制剂,IC50 为 6.5 μM。Shikonin 是一种特异的丙酮酸激酶 M2 (PKM2) 抑制剂,还可以抑制 TNF-αNF-κB途径。Shikonin 通过抑制糖酵解降低外泌体 (exosome) 的分泌。Shikonin 抑制 AIM2炎性体活化。
  • HY-N0182
    Fisetin Inhibitor ≥98.0%
  • HY-P0224
    N-Formyl-Met-Leu-Phe Inhibitor 99.46%
    N-Formyl-Met-Leu-Phe (fMLP; N-Formyl-MLF) 是一种趋化肽和N-甲酰基肽受体 (FPR) 的特异性配体。报道显示N-Formyl-Met-Leu-Ph 可抑制 TNF-alpha 的分泌。
  • HY-P9908
    Adalimumab Inhibitor 98.12%
    Adalimumab 是一种人源的单克隆 IgG1 抗体,靶向肿瘤坏死因子α (TNF-α)。
  • HY-N0066
    Eucalyptol Inhibitor ≥98.0%
    Eucalyptol 是 5-HT3 受体, 钾通道, TNF-αIL-1β 的抑制剂。
  • HY-117082
    UTL-5g Inhibitor 98.97%
    UTL-5g (GBL-5g) 是一种抗炎性 TNF-α 抑制剂,具有化学保护和肝脏放射保护作用。UTL-5g 通过抑制 TNF-α 等因子降低顺铂引起的肝毒性、肾毒性和骨髓毒性。
  • HY-P3149B
    LEESGGGLVQPGGSMK acetate,一种蛋白水解肽,是 Infliximab 的一种成分,可用于 Infliximab 的定量分析。Infliximab 是一种与 TNF-α 特异性结合的嵌合单克隆 IgG1 抗体。
  • HY-110203
    R-7050 Antagonist 99.26%
    R-7050 (TNF-α Antagonist III) 是一种肿瘤坏死因子受体 (TNFR) 拮抗剂,对 TNFα 具有更高选择性。
  • HY-13812
    QNZ Inhibitor ≥98.0%
    QNZ (EVP4593) 强抑制 NF-κB 转录激活和 TNF-α 产生,IC50 分别为 11 和 7 nM。QNZ (EVP4593) 是一种保护神经的钙池操纵的钙通道 (SOC) 抑制剂。
  • HY-P9970
    Infliximab Inhibitor
    Infliximab (Avakine) 是一种与 TNF-α 特异性结合的嵌合单克隆 IgG1 抗体。Infliximab 可阻止 TNF-α 与 TNF-α 受体 1 (TNFR1) 和 TNFR2 的相互作用。Infliximab 可用于自身免疫,慢性炎症性疾病和糖尿病神经病变的研究。
  • HY-N0633
    Muscone Inhibitor ≥98.0%
    Muscone 是中药麝香的主要活性单体。Muscone 抑制 NF-κBNLRP3 炎性小体的活化。Muscone 显着降低炎性细胞因子 (IL-1βTNF-αIL-6) 水平,并最终改善心脏功能和存活率。
  • HY-111255
    SPD304 Inhibitor ≥99.0%
    SPD304 是肿瘤坏死因子 α (TNF-α) 的选择性抑制剂,能够促进肿瘤坏死因子三聚体的分离,从而阻断其与受体间的相互作用。SPD304 体外抑制肿瘤坏死因子 α 和受体 1 间结合的 IC50 值为 22 µM。
  • HY-108847
    Etanercept Inhibitor
    Etanercept 是一种结合肿瘤坏死因子 (TNF) 的二聚体融合蛋白,作为 TNF 抑制剂。Etanercept 竞争性地抑制 TNF-α 和 TNF-β 与细胞表面 TNF 受体的结合,使肿瘤坏死因子在生物学上失去活性。Etanercept 对风湿性关节炎、幼年特发性关节炎和斑块性银屑病有效。
  • HY-N0029
    Forsythoside B 99.99%
    Forsythoside B 是传统中药植物独一味的叶子中分离的苯乙醇苷。独一味可用于炎症疾病和促进血液循环的研究。Forsythoside B 可抑制 TNF-alphaIL-6IκB, 调节 NF-κB
  • HY-119307
    Apratastat Inhibitor ≥99.0%
    Apratastat 是一种口服活性,有效且可逆的肿瘤坏死因子-α 转换酶 TACE 和基质金属蛋白酶 MMPs 的双重抑制剂。Apratastat 可以在体外,离体和体内有效抑制 TNF-α 的释放,体外和离体的 IC50 分别为 144 ng/mL和 81.7 ng/mL。
  • HY-N0722
    Neochlorogenic acid Inhibitor 99.07%
    Neochlorogenic acid 是在干果和其他植物中发现的一种天然多酚化合物。Neochlorogenic acid 抑制 TNF-αIL-1β 产生。 Neochlorogenic acid 抑制 iNOSCOX-2 蛋白表达。Neochlorogenic acid 还抑制磷酸化的 NF-κB p65p38 MAPK 活化。
  • HY-N0604
    Ginsenoside Rh1 Inhibitor ≥98.0%
    Ginsenoside Rh1 (Prosapogenin A2) 抑制 PPAR-γTNF-αIL-6IL-1β 的表达。
  • HY-N0509
    Astilbin Inhibitor 99.22%
    Astilbin 是一种黄酮类化合物,可增强 NRF2 活化。Astilbin 还抑制 TNF-α 表达和 NF-κB 活化。
  • HY-15509A
    Semapimod tetrahydrochloride Inhibitor
    Semapimod tetrahydrochloride (CNI-1493) 是促炎细胞因子产生 (proinflammatory cytokine) 的抑制剂,可抑制TNF-αIL-1βIL-6。Semapimod tetrahydrochloride 抑制巨噬细胞 p38 MAPK 和一氧化氮生成。Semapimod tetrahydrochloride 抑制 TLR4 信号 (IC50≈0.3 μM)。Semapimod tetrahydrochloride 在多种炎症和自身免疫性疾病中具有潜在的作用。

Following the binding of TNF to TNF receptors, TNFR1 binds to TRADD, which recruits RIPK1, TRAF2/5 and cIAP1/2 to form TNFR1 signaling complex I; TNFR2 binds to TRAF1/2 directly to recruit cIAP1/2. Both cIAP1 and cIAP2 are E3 ubiquitin ligases that add K63 linked polyubiquitin chains to RIPK1 and other components of the signaling complex. The ubiquitin ligase activity of the cIAPs is needed to recruit the LUBAC, which adds M1 linked linear polyubiquitin chains to RIPK1. K63 polyubiquitylated RIPK1 recruits TAB2, TAB3 and TAK1, which activate signaling mediated by JNK and p38, as well as the IκB kinase complex. The IKK complex then activates NF-κB signaling, which leads to the transcription of anti-apoptotic factors-such as FLIP and Bcl-XL-that promote cell survival. 


The formation of TNFR1 complex IIa and complex IIb depends on non-ubiquitylated RIPK1. For the formation of complex IIa, ubiquitylated RIPK1 in complex I is deubiquitylated by CYLD. This deubiquitylated RIPK1 dissociates from the membrane-bound complex and moves into the cytosol, where it interacts with TRADD, FADD, Pro-caspase 8 and FLIPL to form complex IIa. By contrast, complex IIb is formed when the RIPK1 in complex I is not ubiquitylated owing to conditions that have resulted in the depletion of cIAPs, which normally ubiquitylate RIPK1. This non-ubiquitylated RIPK1 dissociates from complex I, moves into the cytosol, and assembles with FADD, Pro-caspase 8, FLIPL and RIPK3 (but not TRADD) to form complex IIb. For either complex IIa or complex IIb to prevent necroptosis, both RIPK1 and RIPK3 must be inactivated by the cleavage activity of the Pro-caspase 8-FLIPL heterodimer or fully activated caspase 8. The Pro-caspase 8 homodimer generates active Caspase 8, which is released from complex IIa and complex IIb. This active Caspase 8 then carries out cleavage reactions to activate downstream executioner caspases and thus induce classical apoptosis. 


Formation of the complex IIc (necrosome) is initiated either by RIPK1 deubiquitylation mediated by CYLD or by RIPK1 non-ubiquitylation due to depletion of cIAPs, similar to complex IIa and complex IIb formation. RIPK1 recruits numerous RIPK3 molecules. They come together to form amyloid microfilaments called necrosomes. Activated RIPK3 phosphorylates and recruits MLKL, eventually leading to the formation of a supramolecular protein complex at the plasma membrane and necroptosis [1][2].


[1]. Brenner D, et al. Regulation of tumour necrosis factor signalling: live or let die.Nat Rev Immunol. 2015 Jun;15(6):362-74. 
[2]. Conrad M, et al. Regulated necrosis: disease relevance and therapeutic opportunities.Nat Rev Drug Discov. 2016 May;15(5):348-66. 

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