16
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Cat. No. | Product Name | Target | Signaling Pathways |
---|---|---|---|
T41027 |
MLKL-IN-2
|
MLK | MAPK |
MLKL-IN-2 是一种 MLKL 抑制剂,具有潜在的肿瘤活性,可用于研究细胞坏死相关疾病。 | |||
T60885 |
MLKL-IN-1
|
Others | Others |
MLKL-IN-1 是MLKL 的共价抑制剂,Kd 值为 50 μM。 | |||
T73279 |
MLKL-IN-5
|
Others | Others |
MLKL-IN-5 是一种有效的MLKL 抑制剂,可介导细胞坏死性凋亡。 | |||
T79731 |
MLKL-IN-6
|
Necroptosis | Apoptosis |
MLKL-IN-6(compound P28)是一种针对Mixed Lineage Kinase domain-like(MLKL)的混合谱系激酶抑制剂,具有抗纤维化的潜力。它能够抑制MLKL的磷酸化和寡聚化,从而抑制细胞坏死、免疫细胞死亡,并减少粘附因子的表达。MLKL-IN-6展现出低细胞毒性,并可抑制肝星状细胞的激活,从而降低肝纤维化标志物的水平。 | |||
T79831 |
PROTAC MLKL Degrader-1
|
Others | Others |
PROTACMLKL Degrader-1 (Compound 36) 为MLKL的PROTAC靶向降解剂,具有超过90%的Dmax效率。该化合物构成包含了修饰后的CRBN配体、linker 及 Lenalidomide 接头片段,能有效消除TSZ坏死模型中的细胞死亡。 | |||
T7697 |
BIX-01294
|
Histone Methyltransferase; Autophagy | Autophagy; Chromatin/Epigenetic |
BIX-01294 是高度选择性的G9a 和GLP 组蛋白甲基转移酶可逆抑制剂。它通过与底物赖氨酸残基 N 端的氨基酸竞争结合来抑制 G9a/GLP,可诱导坏死性凋亡和自噬,具有抗肿瘤活性。 | |||
T1959 |
BIX-01294 trihydrochloride
BIX 01294 |
Histone Methyltransferase; Autophagy | Autophagy; Chromatin/Epigenetic |
BIX-01294 trihydrochloride 是可逆且高度选择性的G9a 和GLP 组蛋白甲基转移酶抑制剂,IC50分别为 1.9 μM 和 0.7 μM。它可诱导坏死性凋亡和自噬,具有抗肿瘤活性。它通过与底物赖氨酸残基 N 端的氨基酸竞争结合来抑制 G9a/GLP。 | |||
T11520 |
GW806742X
|
MLK; VEGFR | Angiogenesis; MAPK; Tyrosine Kinase/Adaptors |
GW806742X 是ATP 模拟物,是MLKL 抑制剂,可结合 MLKL 假激酶结构域,Kd 值为 9.3μM。它对VEGFR2的IC50为 2 nM,延缓 MLKL 膜移位并抑制坏死。 | |||
T7129 |
(E/Z)-Necrosulfonamide
N-[4-[[(3-甲氧基吡嗪基)氨基]磺酰基]苯基]-3-(5-硝基-2-噻吩基)-2-丙烯酰胺 |
MLK | MAPK |
(E/Z)-Necrosulfonamide 是一种新型的 MLKL 抑制剂。 | |||
T6904 |
Necrosulfonamide
(E)-Necrosulfonamide |
MLK | MAPK |
Necrosulfonamide ((E)-Necrosulfonamide) 是一种坏死性凋亡抑制剂,通过选择性靶向(MLKL),可阻止 MLKL-RIP1-RIP3 坏死小体复合体与其下游效应子相互作用。MLKL 是诱导坏死过程中 RIP3 的重要底物。 | |||
T81268 |
RIPK1-IN-17
|
RIP kinase | Apoptosis; NF-κB |
RIPK1/3-IN-1(Compound 10)是RIPK1与RIPK3的抑制剂,其通过抑制RIPK1、RIPK3及MLKL的磷酸化作用,特异性地抑制坏死性凋亡。 | |||
T78784 |
RIPK3-IN-3
|
Others | Others |
RIPK3-IN-3(化合物20)是一种针对受体相互作用蛋白激酶RIPK3的选择性抑制剂,其IC50为10 nM。它通过抑制p-MLKL的寡聚化作用来阻止RIPK3介导的MLKL磷酸化以及随后的坏死性凋亡。此外,RIPK3-IN-3还能降低CXCL5的分泌,并抑制AsPC-1细胞的迁移和侵袭。 | |||
T74680 |
NecroIr1
|
Others | Others |
NecroIr1 是一种铱 (III) 复合物,是顺铂 (Cisplatin) 耐药肺癌细胞 (A549R) 的坏死诱导剂。NecroIr1 选择性积累在线粒体中,导致氧化应激和线粒体膜电位 (MMP) 的损失。NecroIr1 能够激活受体相互作用的丝氨酸苏氨酸激酶 3 (RIPK3) 和混合谱系激酶结构域样假激酶 (MLKL),调节CDK4表达。 | |||
T74681 |
NecroIr2
|
Others | Others |
NecroIr2 是一种铱 (III) 复合物,是顺铂 (Cisplatin) 耐药肺癌细胞 (A549R) 的坏死诱导剂。NecroIr2 选择性积累在线粒体中,导致氧化应激和线粒体膜电位 (MMP) 的损失。NecroIr2 能够激活受体相互作用的丝氨酸苏氨酸激酶 3 (RIPK3) 和混合谱系激酶结构域样假激酶 (MLKL),调节CDK4表达。 | |||
T72551 |
Antitumor agent-87
|
Others | Others |
Antitumor agent-87 是一种抗肿瘤剂,具有抗增殖活性,诱导细胞周期停滞。 | |||
T17010 |
TC13172
|
Others | Others |
TC13172 is an inhibitor of mixed lineage kinase domain-like protein (EC50: 2 nM for HT-29 cells). |
Cat. No. | Product Name | Species | Expression System |
---|---|---|---|
TMPH-01694 |
MLKL Protein, Human, Recombinant (E. coli, His)
MLKL,Mixed lineage kinase domain-like protein |
Human | E. coli |
Pseudokinase that plays a key role in TNF-induced necroptosis, a programmed cell death process. Does not have protein kinase activity. Activated following phosphorylation by RIPK3, leading to homotrimerization, localization to the plasma membrane and execution of programmed necrosis characterized by calcium influx and plasma membrane damage. In addition to TNF-induced necroptosis, necroptosis can also take place in the nucleus in response to orthomyxoviruses infection: following activation by ZB... | |||
TMPH-02876 |
RIPK1 Protein, Mouse, Recombinant (His)
Cell death protein RIP,Receptor-interacting protein 1,Ripk1,... |
Mouse | E. coli |
Serine-threonine kinase which is a key regulator of TNF-mediated apoptosis, necroptosis and inflammatory pathways. Exhibits kinase activity-dependent functions that regulate cell death and kinase-independent scaffold functions regulating inflammatory signaling and cell survival. Has kinase-independent scaffold functions: upon binding of TNF to TNFR1, RIPK1 is recruited to the TNF-R1 signaling complex (TNF-RSC also known as complex I) where it acts as a scaffold protein promoting cell survival, i... |