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Osimertinib (AZD-9291) 是一种 EGFR 三代抑制剂，抑制二代 EGFR 抑制剂产生的 T790M 耐药突变，具有不可逆性和口服活性。Osimertinib 具有抗肿瘤活性，用于治疗 EGFR 突变的非小细胞肺癌。

Osimertinib mesylate (AZD-9291 mesylate) 是一种 EGFR 三代抑制剂，抑制二代 EGFR 抑制剂产生的 T790M 耐药突变，具有不可逆性和口服活性。Osimertinib mesylate 具有抗肿瘤活性，用于治疗 EGFR 突变的非小细胞肺癌。

TAS6417 是一种高效的、具有口服活性的 EGFR 突变型抑制剂，可独特的结合到 EGFR 铰链区的 ATP 结合位点，其 IC50值为 1.1-8.0 nM。

D609 (Tricyclodecan-9-yl-Xanthogenate) 具有广泛的生物活性，包括抗氧化、抗凋亡、抗胆碱能、抗肿瘤、抗炎、抗病毒、抗增殖和神经保护活性。D609 通过引起磷脂酰胆碱 (PC) 特异性磷脂酶 C (PC-PLC) 和鞘磷脂合酶 (SMS) 的竞争性抑制来发挥作用。

YS-67 是一种可口服且具有选择性和高效性的 EGFR 抑制剂，具有抗肿瘤活性，抑制 p-EGFR 和 p-AKT，抑制 A549、PC-9 和 A431 细胞的增殖。YS-67在 G0/G1 期阻止细胞周期进程并诱导细胞凋亡，可用于研究非小细胞肺癌。

PON-PC, an oxidized phospholipid with a 9-carbon fatty acyl chain ending in an aldehyde at the sn-2 position, arises from the oxidation of palmitoyl oleoyl phosphatidylcholine (POPC) or through interaction with ozone in pulmonary surfactant. It is found in oxidized LDL. At a 40 µM concentration, PON-PC diminishes the production of TNF-α, nitric oxide (NO), and NADP+ in primary mouse alveolar macrophages and lowers the bactericidal capability of RAW 264.7 cells. Additionally, levels of PON-PC increase in the bronchoalveolar lavage fluid (BALF) of mice exposed to cigarette smoke or in older mice.

C26:0 Lyso PC-d9 是 C26:0 Lyso PC 的氘代化合物。C26:0 Lyso PC 的 CAS 号为 1213783-80-2。

Ensartinib (X-396) is a potent and dual ALK MET inhibitor with IC50s of <0.4 nM and 0.74 nM, respectively. The ability of Ensartinib (X-396) to inhibit the growth of different cancer cell lines harboring ALK fusions or point mutations is tested. Ensartinib is potent in H3122 lung cancer cells harboring EML4-ALK E13;A20 (IC50: 15nM). Ensartinib is also potent in H2228 lung cancer cells harboring EML4-ALK E6a b; A20 (IC50: 45 nM). Furthermore, X-376 is potent in SUDHL-1 lymphoma cells harboring NPM-ALK (IC50: 9 nM). X-376 also inhibits SY5Y neuroblastoma cells harboring ALK F1174L, MKN-45 gastric carcinoma cells harboring MET dependent, HepG2 cells and PC-9 lung cancer cell lines harboring EGFR exon 19 del with IC50s of 68 nM, 156 nM, 9.644 μM and 2.989 μM, respectively[1]. The effects of Ensartinib (X-396) in vivo against H3122 xenografts are examined. A pharmacokinetic study reveals that Ensartinib shows substantial bioavailability and moderate half-lives in vivo. Nude mice harboring H3122 xenografts are treated with Ensartinib at 25mg kg bid. Ensartinib significantly delays the growth of tumors compared to vehicle alone. In the xenograft experiments, Ensartinib appears well-tolerated in vivo. Mouse weight is unaffected by Ensartinib treatment. Drug-treated mice appear healthy and do not display any signs of compound related toxicity. To further assess potential side effects of Ensartinib, additional systemic toxicity and toxico-kinetic studies are performed in Sprague Dawley (SD) rats. Following 10 days of repeated oral administration of Ensartinib at 20, 40, 80 mg kg in SD rats, all animals survive to study termination. The no significant toxicity (NST) levels are determined to be 80mg kg for Ensartinib. At NST levels, Ensartinib achieves an AUC of 66 μM×hr and a Cmax of 7.19 μM[1]. [1]. Lovly CM, et al. Insights into ALK-driven cancers revealed through development of novel ALK tyrosine kinaseinhibitors. Cancer Res. 2011 Jul 15;71(14):4920-31.

PROTACEGFRdegrader 8 (T-184) 是一种能够定向降解EGFR的PROTACEGFR降解剂，其在HCC827细胞中的DC50为15.56 nM。该化合物有效抑制多种肺癌细胞系，包括H1975、PC-9和HCC827，其IC50分别为7.72 nM、121.9 nM和14.21 nM。PROTACEGFRdegrader 8 主要用于研究非小细胞肺癌（NSCLC）。

EGFR-IN-117（Compound 8h）能够对EGFR突变进行靶向抑制，并诱导癌细胞凋亡(apoptosis)。该化合物在H1975、PC-9 以及变异细胞BaF3-EGFRL858R T790M C797S和BaF3–C797S Del19 T790M中表现出显著的抑制活性，其IC50值分别为13 nM、19 nM、1.2 nM和1.3 nM。此外，EGFR-IN-117在小鼠模型上也展现了其抗肿瘤效果。

B-Raf IN 9 (compound 8b) 是有效的B-Raf 抑制剂（IC50= 24.79 nM）。B-Raf IN 9 将细胞周期阻滞于 G2 M 期，诱导凋亡。B-Raf IN 9 对人前列腺癌 PC-3 细胞表现出较强的抗肿瘤活性（IC50= 7.83 μM）。

ASK120067 is a potent and orally active inhibitor of EGFRT790M (IC50:0.3 nM) with selectivity over EGFRWT (IC50:6.0 nM). ASK120067 is a third-generation EGFR-TKI for the research of non-small cell lung cancer (NSCLC)[1]. In the in vitro kinase assay ASK120067 potently inhibits the EGFR L858R T790M and EGFR T790M resistant mutants with IC50 values of 0.3 nM and 0.5 nM, respectively, as well as the EGFRexon19del sensitizing mutant (IC50= 0.5 nM). The 50 of ASK120067 against wild-type EGFR (EGFRWT) is 6 nM[1].ASK120067 selectively inhibits the growth of EGFR-mutant cell lines and exhibits potent antiproliferative activity in the mutant EGFR NSCLC cells, with IC50 values of 12 nM, 6 nM and 2 nM against NCI-H1975 (T790M mutation), PC-9, and HCC827 cells (sensitizing mutations), respectively. However, it shows moderate or weak anti-growth activities in A431, LoVo and A549 cells (EGFRWT), with IC50 values ranging from 338 nM to 1541 nM[1].ASK120067 (0.1-100 nM) inhibits the phosphorylation of EGFR at Tyrosine residue 1068 and its downstream signaling proteins AKT and ERK in NCI-H1975 cells (EGFRL858R T790M) even at low dosage (0.1-1 nM). Additionally, ASK120067 inhibits p-EGFR and p-Akt and p-erk in EGFR WT A431 cell until the concentration reaches 10 to 100 nM[1]. ASK120067 (oral gavage; 5-20 mg kg; once daily; 21 days) results in significantly regressed tumor growth, with a tumor growth inhibition (TGI) rate of 85.7%, and administration of 10 mg kg ASK120067 causes dramatic tumor shrinkage with a TGI rate of 99.3%, exhibiting a similar potency with Osimertinib[1]. [1]. Tao Zhang, et al. Discovery of a novel third-generation EGFR inhibitor and identification of a potential combination strategy to overcome resistance. Mol Cancer. 2020 May 13;19(1):90.