pdgf-receptor

AG 1295 是选择性血小板衍生生长因子受体酪氨酸激酶抑制剂。它能抑制 PDGFR 的自磷酸化，对 EGF 受体的自磷酸化无影响。

CYM50260 是有效的、强选择性的鞘氨醇-1-磷酸 4 受体 (S1P4-R) 激动剂 (EC50= 45 nM)，对 S1P1-R，S1P2-R，S1P3-R 和 S1P5-R 无活性。

AG-494 (Tyrphostin B48) 是一种高效、选择性的 EGFR 酪氨酸激酶抑制剂，IC50为0.7 μM。它阻断 Cdk2 的激活并抑制 EGF 依赖的 DNA 合成。它抑制 EGFR、ErbB2、HER1-2 和 PDGF-R 的自磷酸化，IC50为 1.1、39、45 和 6 μM。

PDGFR Tyrosine Kinase Inhibitor III (PDGF Receptor Tyrosine Kinase Inhibitor III) (PDGF Receptor Tyrosine Kinase Inhibitor III)是一种多激酶抑制剂，可抑制 PDGFR、EGFR、FGFR、PKA 和 PKC 等。PDGFR Tyrosine Kinase Inhibitor III 可用于肌萎缩侧索硬化症的研究。

KN1022是血小板衍生生长因子（PDGF）受体磷酸化抑制剂，IC50为0.26μM。

WQ-C-401 是一种抗PDGFR的口服抑制剂，其作用机制是通过浓度依赖性抑制PDGFR自身的磷酸化，从而抑制细胞增殖。该化合物对PDGFRαY849和PDGFRβY1021的磷酸化具有较强的抑制效果，EC50值分别为3.5和5.8 nM。此外，WQ-C-401能够抑制PDGF-BB引起的ERK1 2磷酸化，有效阻止PASMCs的增殖和迁移，减少胶原 I 的合成并提升α-SMA的表达，有助于防止肺血管重塑。该化合物在肺动脉高压研究领域显示出潜在应用价值。

2-Methyl-3-phenylquinoxaline (compound 38) 作为一种有效的血小板衍生生长因子受体酪氨酸激酶 (PDGF-RTK) 抑制剂，对完整细胞中的PDGFR激酶显示出抑制活性，其半抑制浓度 (IC50) 超过 100 μM。

ABT-869是一种针对所有血管内皮生长因子(VEGF)和血小板源生长因子(PDGF)受体酪氨酸激酶(RTKs)的新型ATP竞争性抑制剂。A-849529是其亲水性代谢产物，包含羧基和氨基团。

AG 370 是一种吲哚 tyrphostin，是一种有效的PDGF 诱导的有丝分裂抑制剂，IC50值为 20 μM。AG 370 对 EGF 受体的抑制作用较弱。

PD-161570 是一种有效的 ATP 竞争性人 FGF-1 受体抑制剂，IC50 为 39.9 nM，Ki 为 42 nM。它还是骨形态发生蛋白 (BMPs) 和TGF-β信号抑制剂。它抑制PDGF 刺激的自磷酸化和FGF-1受体磷酸化，IC50分别为 450 和 622 nM。它抑制 PDGFR、EGFR 和 c-Src 酪氨酸激酶，IC50 值分别为 310、240 和 44 nM。

Vascular endothelial growth factor receptor 2 (VEGFR2, also known as KDR and FLK1) is a receptor tyrosine kinase that regulates angiogenesis, vascular development, and embryonic hematopoiesis in response to VEGF isoforms A, C, and D. VEGFR2 kinase inhibitor II is a reversible, cell-permeable inhibitor of VEGFR2's kinase activity (IC50 = 70 nM). It less potently inhibits the platelet-derived growth factor receptor β (PDGFRβ; IC50 = 920 nM) and related receptor and non-receptor tyrosine kinases. VEGFR2 kinase inhibitor II blocks the growth of human umbilical vein endothelial cells stimulated with either VEGF or PDGF (IC50s = 110 nM and 2 μM, respectively).

Ansornitinib (ANG-3070) 是一种具有口服活性的 KDR 和 PDGF 受体抑制剂，具有抗纤维化活性，抑制血小板衍生生长因子受体 (PDGFR) 和血管内皮生长因子受体 (VEGFR2)，可用于研究异常或过度纤维化引起的疾病。

Tyrphostin AG1296 (Tyrphostin AG 1296) 抑制人PDGF α和β受体以及相关干细胞因子受体的信号传导，是一种选择性血小板衍生生长因子受体抑制剂，IC50值为 0.8 μM。

The growth factors, platelet-derived growth factor (PDGF) and basic fibroblast growth factor (bFGF) play major roles in enhanced smooth muscle cells growth in rodent blood vessels after vascular injury. Tyrosine kinase inhibition has been shown to be effective in blocking tyrosine phosphorylation at the PDGF and bFGF receptors in cultured fibroblast and vascular smooth muscle cells which in turn inhibits their proliferation[1]. CGP 53716 is a specific PDGFR tyrosine kinase inhibitor on SMC (smooth muscle cell) proliferation and migration in vitro and in neointimal formationin vivo[3]. CGP 53716 inhibited serum-induced cell growth in RASMC (rat aortic smooth muscle cells). And it completely blocked PDGF-BB tyrosine receptor autophosphorylation in RASMC and 3T3 cells, PDGF-BB-induced phosphorylation of mitogen-activated protein kinase at 1 μM in RASMC and inhibited PDGF-BB-induced c-Fos protein expression at 1 μM in RASMC; consistent with inhibition of PDGF-BB-induced DNA synthesis. Further, CGP 53716 inhibited PDGF-BB-, bFGF- and EGF-induced DNA synthesis in a concentration-dependent manner in each cell line. And it showed a 2- to 4-fold selectivity for PDGF-BB-stimulated DNA synthesis over bFGF or EGF in RASMC or 3T3 cells[1]. CGP 53716 inhibited dose dependently tyrosine phosphorylation of both the known PDGFRs: the PDGFR-α and PDGFR-β. After rat carotid artery ballooning injuryin vivo, the migration of alpha-actin-positive cells on the luminal side of internal elastic lamina was decreased with 50 mg kg day of CGP 53716 from 38 ± 10 (control group) to 4 ± 2. Intima media ratio was inhibited by 40% after 14 days in the CGP 53716-treated group (P=0.028) after rat aortic denudation[3].

SU 5402 是多靶点受体酪氨酸激酶抑制剂，能够抑制VEGFR2 (IC50:20 nM)，FGFR1 (IC50:30 nM)，PDGFRβ (IC50:510 nM)。

Rinucumab (REGN 2176) 是一种抗血小板衍生生长因子（PDGF）的 IgG4 类单克隆抗体，通过与 PDGF-β 受体结合发挥作用，可用于研究年龄相关性黄斑变性。