cancer-initiating

PTC-209 是特定的BMI-1抑制剂，不可逆转地损害结直肠癌起始细胞，在 HEK293T 细胞系中的IC50为 0.5 μM。它有抗骨髓瘤活性并损害肿瘤微环境。

YHO-13351 是多药物转运蛋白 （ABCG2） 抑制剂，是丙烯腈衍生物，诱导癌症干细胞 起始样侧群体细胞对伊立替康敏感。

Darinaparsin is a dimethylated arsenic linked to glutathione. It is cytotoxic to DU145, LNCaP, and PC3 prostate cancer cells (IC50s = 5-10 µM) and patient-derived primary prostate cancer cells (IC50s = 2.5-20 µM), as well as Jurkat T cell lymphoma and L540 Hodgkin lymphoma cells (IC50s = 2.7 and 1.3 µM, respectively). [1][2] It decreases the tumor-initiating subpopulation in DU145 and PC3 cells and halts the cell cycle in the G2 M phase. Darinaparsin decreases transcription of Gli-2, a transcription factor that mediates Sonic hedgehog signaling, when used at a concentration of 1.5 but not 3 µM. It decreases SHP1 phosphatase activity and increases ERK phosphorylation. [2] Darinaparsin reduces tumor growth in DU145 and PC3 prostate cancer mouse xenograft models when administered at a dose of 100 mg kg every other day.[1]

Becatecarin is a water-soluble, diethylaminoethyl analog of the antineoplastic antibiotic rebeccamycin. It intercalates into DNA, stabilizing the DNA-topoisomerase complex. This results in the potent catalytic inhibition of both topoisomerases I and II, initiating DNA cleavage and apoptosis. Becatecarin, alone or in combination with other compounds, has anti-cancer as well as myelosuppressive effects in vivo. It is also a transport substrate of the ATP-binding cassette (ABC) transporter ABCG2.

Roy-Bz is a potent and selective activator of protein kinase C delta (PKCδ). It effectively inhibits proliferation in colon cancer cells by initiating a mitochondrial apoptotic pathway that relies on PKCδ and involves the activation of caspase-3.

PTC-209 hydrobromide (PTC-209 HBr) 是一种特定的BMI-1抑制剂，能不可逆转地损害结直肠癌起始细胞，也可损害肿瘤微环境，有抗骨髓瘤活性。它在 HEK293T 细胞系中的IC50为 0.5 μM。

fac-[Re(CO)3(L3)(H2O)][NO3]（简称compound 3），是一种与线粒体功能障碍相关的抗前列腺癌剂。这种铼(I)三羰基水配合物对前列腺癌细胞系(PC-3)表现出显著的细胞毒性，其IC50值为0.32 μM。研究表明，fac-[Re(CO)3(L3)(H2O)][NO3]主要在线粒体中积聚，能够降低PC-3细胞的ATP生成，进而触发细胞副凋亡(paraptosis)机制，而不通过引发坏死、凋亡或自噬途径作用。

Nε-(1-Carboxymethyl)-L-lysine (CML), an advanced glycation end product (AGE), is formed through the oxidative modification of glycated proteins under conditions of oxidative stress.1,2,3 Its levels escalate with age, diabetes, cancer, vascular diseases, and various pathologies associated with oxidative stress.1,4,5 CML interacts with the membrane-bound receptor for AGEs (RAGE), initiating signaling via MAPKs and NF-κB pathways. Conversely, a truncated version of RAGE generates a soluble protein that sequesters CML, thereby diminishing this signaling.6,7

NL13作为一种Polo样激酶4 (PLK4) 抑制剂，具有2.32 μM的IC50值。在抑制前列腺癌细胞线PC3和DU145方面，其IC50值分别为3.51 μM和2.53 μM。该化合物能够引起AKT信号通路的失活，并通过下调CCNB1 CDK1，导致G2 M细胞周期阻滞。同时，NL13通过caspase-9 caspase-3切割，触发细胞凋亡（apoptosis）。此外，NL13在小鼠模型中已证实能有效抑制前列腺癌肿瘤的生长。