Erlotinib (NSC-718781) is an EGFR inhibitor (IC50: 2 nM). It is used for the treatment of non-small cell lung cancer.

Erlotinib is an epidermal growth factor receptor inhibitor. Erlotinib binds in a reversible fashion to the adenosine triphosphate (ATP) binding site of the receptor.

Erlotinib Hydrochloride inhibits purified EGFR kinase with an IC50 of 2 nM. Erlotinib D6 hydrochloride a deuterium labeled Erlotinib Hydrochloride.

Erlotinib is a directly acting inhibitor EGFR tyrosine kinase inhibitor with an IC50 of 2 nM for human EGFR. Erlotinib D6 is a deuterium labeled Erlotinib .

Desmethyl Erlotinib hydrochloride (OSI 420) is an active metabolite of erlotinib which is an orally active EGFR tyrosin kinase inhibitor with IC50 of 2 and 20 nM for human EGFR and EGFR autophosphorylation in tumor cells.

Desmethyl Erlotinib (CP-473420) is the active metabolite of Erlotinib (EGFR inhibitor with IC50 of 2 nM).

Erlotinib hydrochloride (NSC 718781) is an EGFR inhibitor (IC50: 2 nM). It is used for the treatment of non-small cell lung cancer.

CP-457493 is a bio-active chemical.

TD52 dihydrochloride (TD52 2HCl), a derivative of Erlotinib, is a potent and orally active inhibitor of protein phosphatase 2A (CIP2A). It exhibits strong anti-cancer properties by regulating the CIP2A/PP2A/p-Akt signaling pathway, resulting in the induction of apoptosis in triple-negative breast cancer (TNBC) cells. Mechanistically, TD52 dihydrochloride disrupts the binding of Elk1 to the CIP2A promoter, effectively reducing CIP2A levels. Notably, TD52 dihydrochloride demonstrates powerful anti-cancer activity while displaying less inhibition of p-EGFR.

WZ4002-hydroxyl is a WZ4002 derivative or WZ4002 analogue in which methoxy is replaced by hydroxyl and can be detected in 50% of patients with clinical resistance to gefitinib or erlotinib. WZ4002 has a basic chemical skeleton (covalent pyrimidine) that d

4-Chloro-6,7-bis(2-methoxyethoxy)quinazoline is a building block and synthetic intermediate.1,2,3,4,5It has been used as a precursor in the synthesis of receptor tyrosine kinase (RTK) inhibitors, dual RTK and histone deacetylase (HDAC) inhibitors, and anticancer compounds.1,2,3It is also a synthetic intermediate in the synthesis of EGFR inhibitors, including erlotinib , with antiproliferative activity.4,5

CH5164840 is a potent and selective HSP90 inhibitor. CH5164840 showed remarkable antitumor activity against NSCLC cell lines and xenograft models. CH5164840 has potent antitumor activity and is highly effective in combination with erlotinib against NSCLC tumors with EGFR overexpression and mutations.

SB02024 is a VPS34 inhibitor. SB02024 activates cGAS-STING signaling and sensitizes tumors to STING agonist. SB02024 blocked autophagy in vitro and reduced xenograft growth of two breast cancer cell lines, MDA-MB-231 and MCF-7, in vivo. Vps34 inhibitor significantly potentiated cytotoxicity of Sunitinib and Erlotinib in MCF-7 and MDA-MB-231 in vitro in monolayer cultures and when grown as multicellular spheroids. Our data suggests that inhibition of autophagy significantly improves sensitivity to Sunitinib and Erlotinib and that Vps34 is a promising therapeutic target for combination strategies in breast cancer.

TM608 is a potent selective c-Met inhibitor that targets mitochondria and kills erlotinib-resistant lung cancer cells, rapidly accumulates in mitochondria, and inhibits MET activation in high MET expression, erlotinib-resistant HCC827B cells (total cell l

TD52 is an orally active inhibitor of cancerous inhibitor of PP2A (CIP2A). TD52 is an Erlotinib derivative and indirectly reduced CIP2A by disturbing Elk1 binding to the CIP2A promoter.

Erasin, a formidable antagonist to Erlotinib resistance, selectively inhibits STAT3 with an IC50 of 9.7 μM, and STAT1 with an IC50 of 24 μM. It effectively induces apoptosis in cancer cells [1].