Chromeceptin (94G6)是一种 IGF 信号通路的抑制剂，能够抑制肝细胞和 HCC 细胞中 IGF2 的 mRNA 和蛋白水平，同时抑制 AKT 和 mTOR 的磷酸化。

Ceritinib D7是一种选择性、口服有效且具有ATP竞争性的ALK酪氨酸激酶抑制剂，适用于ALK相关的癌症治疗研究。

AG1024 inhibits IGF-1R autophosphorylation with IC50 of 7 μM, less potent to IR with IC50 of 57 μM.

Insulin, Human is a two-chain polypeptide hormone produced by the β-cells of pancreatic islets, it regulates the cellular uptake, utilization, and storage of glucose, amino acids, and fatty acids and inhibits the breakdown of glycogen, protein, and fat.

Insulin (cattle) 是一种胰岛素来源于牛的胰腺，具有降血糖作用。牛胰岛素主要用于糖尿病的治疗和胰岛素替代疗法的研究。

PQ401, a selective insulin-like growth factor-1 receptor blocker, is a diarylurea compound that inhibits IGF1R autophosphorylation with IC50 < 1 μM.

Picropodophyllin (AXL1717) 是一种选择性胰岛素样生长因子-1 受体 (IGF-1R) 抑制剂，IC50 为 1 nM。

Ceritinib（LDK378）是一种选择性、口服可用的、ATP竞争性的ALK酪氨酸激酶抑制剂，IC50为200 pM。Ceritinib（LDK378）还以8、7和23 nM的IC50值抑制IGF-1R、InsR和STK22D。Ceritinib（LDK378）显示出强大的抗肿瘤活性。

Ginsenoside Rg5 is a natural product isolated and purified from the roots of Panax ginseng C. A. Mey. showing anti-inflammatory effect.

BMS-536924 is an ATP-competitive IGF-1R/IR inhibitor with IC50 of 100 nM/73 nM.

AZD-3463 (ALK/IGF1R 抑制剂) 是一种口服活性 ALK/IGF1R 抑制剂，对 ALK 的 Ki 为 0.75 nM。AZD-3463 在神经母细胞瘤细胞中诱导凋亡和自噬。

Linsitinib（OSI-906）是一种高效、选择性和口服可用的IGF-1受体和胰岛素受体（IR）的双重抑制剂，IC50分别为35 nM和75 nM。

NVP-AEW541 (AEW541) 是一种口服活性的胰岛素样生长因子 1 受体 (IGF-1R) 抑制剂，IC50 为 0.15 μM。它还抑制胰岛素受体 (InsR)，IC50 为 0.14 μM，显示出显著的抗肿瘤活性。

XL228 is a protein kinase inhibitor targeting IGF1R, the Aurora kinases, FGFR1-3, ABL and SRC family kinases.

BMS-754807 is a potent and reversible inhibitor of IGF-1R/InsR with IC50 of 1.8 nM/1.7 nM, less potent to Met, Aurora A/B, TrkA/B and Ron, and shows little activity to Flt3, Lck, MK2, PKA, PKC etc.

Teprotumumab是一种人源化IgG1单克隆抗体，通过与IGF1R结合来阻止其与配体结合。Teprotumumab具有用于甲状腺相关眼病研究的潜力。

GSK1904529A is a selective inhibitor of IGF-1R and IR with IC50 of 27 nM and 25 nM, being > 100-fold selective for IGF-1R/InsR than Akt1/2, Aurora A/B,B-Raf, CDK2, EGFR etc.

NT157 treatment resulted in dose-dependent inhibition of IGF1R activation, suppression of IRS protein expression, inhibition of IGF1-induced AKT activation, but increased ERK activation in NT157-treated cells in vitro.