osimertinib

Osimertinib (AZD-9291) is an EGFR third-generation inhibitor that inhibits the T790M resistance mutation produced by second-generation EGFR inhibitors with irreversible and oral activity. Osimertinib has antitumor activity for the treatment of EGFR-mutated non-small-cell lung cancer.

Osimertinib mesylate (AZD-9291 mesylate) is an EGFR third-generation inhibitor that inhibits the T790M resistance mutation produced by second-generation EGFR inhibitors with irreversible and oral activity. Osimertinib mesylate has antitumor activity for the treatment of EGFR-mutated non-small-cell lung cancer.

Osimertinib dimesylate is an irreversible and mutant selective EGFR inhibitor (IC50s: 12 and 1 nM against EGFR L858R and EGFR L858R/T790M).

Mutated EGFR-IN-1 (Osimertinib analog) is a valuable intermediate in designing inhibitors for mutated EGFR, including L858R EGFR, Exon19 deletion activating mutant, and T790M resistance mutant.

Osimertinibdimer is the dimer of Osimertinib. Osimertinib (AZD9291) is a covalent, orally active, irreversible, and mutation-selective EGFR inhibitor, effectively suppressing L858R (IC50=12 nM) and L858R/T790M (IC50=1 nM) EGFR. It addresses resistance to EGFR inhibitors mediated by the T790M mutation in lung cancer.

Osimertinib-D6 is a deuterated compound of Osimertinib. Osimertinib (T2490) has a CAS number of 1421373-65-0. Osimertinib (T2490) is a small molecule tyrosine kinase receptor inhibitor and antineoplastic agent that is used in the therapy of selected forms of advanced non-small cell lung cancer (NSCLC).

Osimertinib-13C,D3 is a deuterated form of Osimertinib (T2490) labeled with 13C. Osimertinib (T2490) (AZD9291) is an orally active, covalent, irreversible EGFR inhibitor with mutation selectivity, effectively inhibiting L858R (IC50=12 nM) and L858R/T790M (IC50=1 nM) EGFR mutations. It addresses resistance to EGFR inhibitors caused by the T790M mutation in lung cancer.

Osimertinib (Standard) is a reference standard for research and analysis in studies involving Osimertinib. Osimertinib (AZD-9291) is an EGFR third-generation inhibitor that inhibits the T790M resistance mutation produced by second-generation EGFR inhibitors with irreversible and oral activity. Osimertinib has antitumor activity for the treatment of EGFR-mutated non-small-cell lung cancer.

Osimertinib-13C,D3 (Standard) is a reference standard of Osimertinib-13C,D3 intended for quantitative analysis, quality control, and related biochemical research applications. Osimertinib-13C,d3 is a deuterated form of Osimertinib labeled with 13C. Osimertinib (AZD9291) is an orally active, covalent, irreversible EGFR inhibitor with mutation selectivity, effectively inhibiting L858R (IC50=12 nM) and L858R/T790M (IC50=1 nM) EGFR mutations. It addresses resistance to EGFR inhibitors caused by the T790M mutation in lung cancer.

Dosimertinib-D3 is a potent, orally active inhibitor of EGFR, known to reduce the expression of p-EGFR and p-ERK proteins, thereby exhibiting antiproliferative and anti-tumor effects. It holds promise for research into non-small-cell lung cancer (NSCLC).

JAK-IN-40 (Compound 46) is an inhibitor of JAK, effectively targeting JAK1, JAK2, and JAK3 with IC50 values of 0.022, 0.759, and 1.601 μM, respectively. It reduces the phosphorylation of STAT3 and inhibits the proliferation of cancer cells Ba/F3 and JAK1-TEL Ba/F3 with GI50 values of 0.614 μM and 0.193 μM. JAK-IN-40 arrests cell cycle progression at the G2/M phase in H1975 and H2087 cells, leading to apoptosis. Additionally, JAK-IN-40 exhibits a synergistic anti-tumor effect when used in combination with Osimertinib.

CDK9-IN-36 (Compound T7) is a potent, selective, and metabolically stable CDK9 inhibitor with an IC50 value of 1.2 nM. It effectively suppresses the proliferation of Osimertinib-resistant NSCLC cells by downregulating Mcl-1, reducing colony formation, and inducing apoptosis. Additionally, CDK9-IN-36 exhibits antitumor activity in xenograft models.

Lenalidomide-acetylene-Br is the PROTAC linker that makes up HJM-561. HJM-561 is an effective, selective, and orally active EGFR PROTAC that can inhibit the triple mutation of EGFR which is resistant to Osimertinib.

ER ligand-14-PEG3-Boc is a conjugate of a target protein ligand and a linker, composed of an estrogen receptor (estrogen receptor) ligand and a corresponding linker. It is used in the synthesis of PROTACs such as ERB-2. ERB-2 shows significant antiproliferative activity against non-small cell lung cancer resistant to Osimertinib.

ER ligand-14 is a ligand for the estrogen receptor (ER). It can serve as a ligand for target proteins in PROTACs and is useful in the development and design of PROTACERβ degraders, such as ERB-2. ERB-2 shows significant anti-proliferative activity against non-small cell lung cancer cells that are resistant to Osimertinib.

SG-55 is a selective, non-competitive, orally active inhibitor of AKR1C3, with an IC50 of 5 nM and a Ki of 10 nM. It has over 2000-fold higher selectivity for AKR1C3 compared to AKR1C1, AKR1C2, and AKR1C4 (>10 μM). SG-55 enhances the NADPH/NADP+ ratio, decreases the GSH/GSSG ratio, and induces DNA double-strand breaks. Additionally, SG-55 can overcome resistance to Osimertinib mediated by the EGFRC797S triple mutation in non-small cell lung cancer (NSCLC).

EGFR-IN-47 (compound 14aj) is a potent, fourth-generation, and orally active EGFR inhibitor. It specifically targets the EGFR L858R/T790M/C797S triple mutation with an IC50 of 0.01 uM. In NSCLC research, EGFR-IN-47 effectively overcomes C797S-mediated resistance to Osimertinib by inhibiting the phosphorylation of EGFR and its downstream mediators, subsequently inducing cell cycle arrest and apoptosis.

DBPR112 is a potent EGFR inhibitor (IC50=487 nM) as a Clinical Candidate for the Treatment of Non-Small Cell Lung Cancer. DBPR112), DBPR112 not only displayed a potent inhibitory activity against EGFRL858R/T790M double mutations but also exhibited tenfold potency better than the third-generation inhibitor, osimertinib,against EGFR and HER2 exon 20 insertion mutations. Overall, pharmacokinetic improvement through lead-to-candidate optimization yielded fourfold oral AUC better that afatinib along with F = 41.5%, an encouraging safety profile, and significant antitumor efficacy in in vivo xenograft models.

Olmutinib is a novel third-generation epidermal growth factor receptor (EGFR) mutation-specific tyrosine kinase inhibitor, used in the treatment of T790M mutation positive non-small cell lung cancer. Olmutinib covalently binds a cysteine residue near the kinase domain of mutant EGFRs to prevent phosphorylation of the receptor. EGFRs are frequently over-expressed in lung cancer and contribute to activation of the phosphoinositide 3-kinase and mitogen-activated protein kinase pathways which both promote cell survival and proliferation. By inhibiting EGFR activation, Olmutinib attenuates the activation of these tumor-promoting pathways. In the first phase I/II clinical study of Osimertinib, 800 mg/ day was chosen as the dose for subsequent studies, and the dose-limiting toxicity and maximum tolerated dose was not reached. Olmutinib received breakthrough therapy designation in the United States in December 2015 and was approved for use in Korea in May 2016.

Rezivertinib analogue 1, a process impurity of osimertinib mesylate, serves as a research tool in the study of non-small cell lung cancer (NSCLC) [1].

Becotatug (JMT101) is a humanised monoclonal antibody targeting EGFR, demonstrating antitumour activity when combined with Osimertinib for treating EGFR-mutated advanced NSCLC.

ONO-7475 is an inhibitor with high specificity for anexelekto and MER tyrosine kinase

LS-106 is an orally active, effective epidermal growth factor receptor (EGFR) inhibitor displaying antitumor activity both in vitro and in vivo. It inhibits the kinase activities of EGFR19del/T790M/C797S and EGFRL858R/T790M/C797S, with IC50 values of 2.4 nmol/L and 3.1 nmol/L, respectively, demonstrating stronger inhibition than Osimertinib. LS-106 induces cell apoptosis (Apoptosis), suppresses the proliferation of tumor cells carrying EGFR19del/T790M/C797S, and results in significant tumor reduction in a C797S mutant xenograft model.

Enapotamab vedotin is an investigational antibody-drug conjugate (ADC) specifically targeting the receptor tyrosine kinase AXL. it consists of a monoclonal antibody linked to the potent microtubule-disrupting agent monomethyl auristatin E (MMAE) and demonstrates significant inhibitory potential against high AXL-expressing non-small cell lung cancer (NSCLC), including tumors with resistance to EGFR inhibitors like Osimertinib.