1. Signaling Pathways
  2. Apoptosis
  3. TNF Receptor

TNF Receptor

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.

Cat. No. Product Name Effect Purity
  • 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。
  • 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-N0182
    Fisetin Inhibitor 98.02%
  • 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-N7699A
    D-Trimannuronic acid Activator
    D-Trimannuronic acid 是一种从海藻中提取的藻酸盐低聚物,可以诱导小鼠巨噬细胞分泌 TNF-α。D-Trimannuronic acid 可用于疼痛和血管性痴呆的研究。
  • HY-N0619A
    cis-Mulberroside A Inhibitor
    cis-Mulberroside A (Mulberroside D) 是 Mulberroside A 的顺式异构体。Mulberroside A 是桑树 (Morus alba L.) 中的主要生物活性成分之一。Mulberroside A 可降低 TNF-αIL-1βIL-6 的表达,抑制 NALP3,caspase-1 和 NF-κB 的激活以及 ERK,JNK 和 p38 的磷酸化 。Mulberroside A 具有抗炎和抗细胞凋亡作用。Mulberroside A 对蘑菇酪氨酸酶 ( tyrosinase) 具有抑制活性,IC50 为 53.6 μM。
  • 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 98.46%
    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-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-N0604
    Ginsenoside Rh1 Inhibitor >98.0%
    Ginsenoside Rh1 (Prosapogenin A2; Sanchinoside B2; Sanchinoside Rh1) 是从 Panax Ginseng 根部分离的。 Ginsenoside Rh1 抑制 PPAR-γTNF-αIL-6IL-1β 的表达。
  • HY-N0722
    Neochlorogenic acid Inhibitor 99.46%
    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-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-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 99.28%
    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-N0509
    Astilbin Inhibitor 99.43%
    Astilbin 是一种黄酮类化合物,可从 Smilax glabra 根茎中分离。Astilbin 增强 NRF2 活化。Astilbin 还抑制 TNF-α 表达和 NF-κB 活化。
  • HY-N1949
    Homoplantaginin Inhibitor 99.90%
    Homoplantaginin是来自中药Salvia plebeia的具有抗炎和抗氧化活性的类黄酮。
  • HY-N0297
    Sinensetin Inhibitor 99.67%
  • HY-19717
    DCVC Inhibitor 99.89%
    DCVC (S-[(1E)-1,2-dichloroethenyl]--L-cysteine) 是一种三氯乙烯 (TCE) 的生物活性代谢产物。DCVC 可抑制病原体刺激的组织培养物中促炎细胞因子 IL-1β,IL-8 和 TNF-α 的释放。
  • HY-N0619
    Mulberroside A Inhibitor 99.75%
    Mulberroside A 是桑树 (Morus alba L.) 中的主要生物活性成分之一。Mulberroside A 可降低 TNF-αIL-1βIL-6 的表达,抑制 NALP3,caspase-1 和 NF-κB 的激活以及 ERK,JNK 和 p38 的磷酸化 。Mulberroside A 具有抗炎和抗细胞凋亡作用。Mulberroside A 对蘑菇酪氨酸酶 ( tyrosinase) 具有抑制活性,IC50 为 53.6 μM。

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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