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Results for "

resistance mutations

" in MedChemExpress (MCE) Product Catalog:

By Targets:	Anaplastic lymphoma kinase (ALK) (2) Apoptosis (1) Aurora Kinase (1) Autophagy (2) c-Met/HGFR (1) EGFR (5) FGFR (2) Flavivirus (1) FLT3 (1) HCV (1) HCV Protease (1) mTOR (1) ROS Kinase (1) Thyroid Hormone Receptor (1) Trk Receptor (1)
By Research Areas:	Cancer (15) Infection (2) Metabolic Disease (1)

Inhibitors & Agonists

Screening Libraries

Natural
Products

Targets Recommended: BCRP P-glycoprotein

Cat. No.	Product Name	Target	Research Areas	Chemical Structure

HY-152292

Zidesamtinib NVL-520	ROS Kinase	Cancer
Zidesamtinib (NVL-520) is a potent, selective, orally active and brain-penetrant inhibitor of diverse ROS1 fusions and **resistance mutations, with IC₅₀s of 0.7 and 7.9 nM for wild-type ROS1 and ROS1 G2032R**, respectively, and spares TRK inhibition. Zidesamtinib can be used for the research of cancer .

HY-153857

PHI-101	FLT3	Cancer
PHI-101 is an orally active FLT3 inhibitor that overcomes resistance to multiple drug-resistant mutations. PHI-101 potently inhibits FLT3 single activating mutations (ITD or TKD mutants) and has inhibitory activity against FLT3 double (ITD/D835Y or ITD/F691L) and triple (ITD/D835Y/F691L) resistance mutations. PHI-101 has potential for research in relapsed or refractory acute myeloid leukemia (AML) .

HY-123159

AKI603	Aurora Kinase	Cancer
AKI603 is an inhibitor of Aurora kinase A (AurA), with an IC₅₀ of 12.3 nM. AKI603 is developed to overcome resistance mediated by BCR-ABL-T315I mutation. AKI603 exhibits strong anti-proliferative activity in leukemic cells .

HY-N8188

Dehydrojuncusol	HCV HCV Protease	Infection
Dehydrojuncusol, a potent HCV inhibitor, targets HCV NS5A and is able to inhibit RNA replication of replicons harboring resistance mutations to anti-NS5A direct-acting antivirals. Dehydrojuncusol significantly inhibits HCV infection when added after virus inoculation of HCV genotype 2a (EC₅₀=1.35 µM) .

HY-146997

TRβ agonist 1	Thyroid Hormone Receptor	Metabolic Disease
TRβ agonist 1 is a selective and mutation-sensitive thyroid hormone receptor β (TRβ) agonist, with an EC₅₀ value of 21 nM. TRβ agonist 1 can be used for researching dyslipidemia, nonalcoholic steatohepatitis (NASH), and resistance to thyroid hormone (RTH) .

HY-135887

ZX-29	Anaplastic lymphoma kinase (ALK) Apoptosis Autophagy	Cancer
ZX-29 is a potent and selective ALK inhibitor with an IC₅₀ of 2.1 nM, 1.3 nM and 3.9 nM for ALK, ALK L1196M and ALK G1202R mutations, respectively. ZX-29 is inactive against EGFR. ZX-29 induces apoptosis by inducing endoplasmic reticulum (ER) stress and overcomes cell resistance caused by an ALK mutation. ZX-29 also induces protective autophagy and has antitumor effect .

HY-147250A

Lirafugratinib hydrochloride RLY-4008 hydrochloride	FGFR	Cancer
Lirafugratinib (RLY-4008) hydrochloride is an orally active, irreversible and highly selective FGFR2 inhibitor with an IC₅₀ of 3 nM. Lirafugratinib hydrochloride covalently binds to Cys491. Lirafugratinib hydrochloride targets FGFR2 primary alterations and resistance mutations and induces tumor regression while sparing other FGFRs .

HY-147250

Lirafugratinib RLY-4008	FGFR	Cancer
Lirafugratinib (RLY-4008) is an orally active, irreversible and highly selective FGFR2 inhibitor with an IC₅₀ of 3 nM. Lirafugratinib covalently binds to Cys491. Lirafugratinib targets FGFR2 primary alterations and resistance mutations and induces tumor regression while sparing other FGFRs .

HY-108230

ALK-IN-12	Anaplastic lymphoma kinase (ALK)	Cancer
ALK-IN-12 is a potent and orally active ALK inhibitor with an IC₅₀ of 0.18 nM. ALK-IN-12 also inhibits IGF1R and InsR (IC₅₀=20.3 and 90.6 nM). Antitumor activities .

HY-109189

Rezivertinib BPI-7711	EGFR	Cancer
Rezivertinib (BPI-7711) is an orally active, highly selective and irreversible third-generation EGFR tyrosine kinase inhibitor (TKI). Rezivertinib exhibits high potency against the common activation EGFR and the resistance T790M mutations. Rezivertinib has excellent central nervous system (CNS) penetration and has antitumor activity .

HY-111373

RapaLink-1 5 Publications Verification	mTOR Autophagy	Cancer
RapaLink-1, the third-generation bivalent mTOR inhibitor, combines Rapamycin (HY-10219) with MLN0128 (HY-13328, a second-generation mTOR kinase inhibitor) by an inert chemical linker. RapaLink-1 shows better efficacy than Rapamycin or mTOR kinase inhibitors (TORKi), potently blocking cancer-derived, activating mutants of mTOR. RapaLink-1 can cross the blood-brain barrier. RapaLink-1 binding to FKBP12 results in targeted and durable inhibition of mTORC1. RapaLink-1 plays an antithrombotic role in antiphospholipid syndrome by improving autophagy. Anticancer activity .

HY-18649B

Galidesivir dihydrochloride BCX4430 dihydrochloride; Immucillin-A dihydrochloride	Flavivirus	Infection
Galidesivir (BCX4430; Immucillin-A) dihydrochloride is a broad-spectrum RNA virus inhibitor that can inhibit Ebola and yellow fever virus (Flavivirus) infections. Galidesivir has potent antiviral activity against tick-borne encephalitis virus (TBEV) and also inhibits the proliferation of many other medically important flaviviruses .

HY-146210

EGFR-IN-50	EGFR	Cancer
EGFR-IN-50 (Compound 9h) is a potent EGFR inhibitor against L858R resistance mutation (TEL-EGFR-L858R-BaF3: GI₅₀=8 nM, TEL-EGFR-T790M-L858R-BaF3: GI₅₀=6.03 μM). EGFR-IN-50 shows anti-proliferative activity to cancer cells .

HY-15456

NVP-BVU972	c-Met/HGFR	Cancer
NVP-BVU972 is an selective and potent Met inhibitor, with an IC₅₀ of 14 nM. NVP-BVU972 also exhibits good anti-proliferative activity against Met with drug-resistant mutations and inhibits phosphorylation. NVP-BVU972 can be used in study of cancer .

HY-112823B

Almonertinib hydrochloride 3 Publications Verification HS-10296 hydrochloride	EGFR	Cancer
Almonertinib (HS-10296) hydrochloride is an orally available, irreversible, third-generation EGFR tyrosine kinase inhibitor with high selectivity for EGFR-sensitizing and T790M resistance mutations. Almonertinib hydrochloride shows great inhibitory activity against T790M, T790M/L858R and T790M/Del19 (IC₅₀: 0.37, 0.29 and 0.21 nM, respectively), and is less effective against wild type (3.39 nM). Almonertinib hydrochloride is used for the research of the non-small cell lung cancer .

HY-112823

Almonertinib 3 Publications Verification HS-10296	EGFR	Cancer
Almonertinib (HS-10296) is an orally available, irreversible, third-generation EGFR tyrosine kinase inhibitor with high selectivity for EGFR-sensitizing and T790M resistance mutations. Almonertinib shows great inhibitory activity against T790M, T790M/L858R and T790M/Del19 (IC₅₀: 0.37, 0.29 and 0.21 nM, respectively), and is less effective against wild type (3.39 nM). Almonertinib is used for the research of the non-small cell lung cancer .

HY-112823A

Almonertinib mesylate 3 Publications Verification HS-10296 mesylate	EGFR	Cancer
Almonertinib (HS-10296) mesylate is an orally available, irreversible, third-generation EGFR tyrosine kinase inhibitor with high selectivity for EGFR-sensitizing and T790M resistance mutations. Almonertinib mesylate shows great inhibitory activity against T790M, T790M/L858R and T790M/Del19 (IC₅₀: 0.37, 0.29 and 0.21 nM, respectively), and is less effective against wild type (3.39 nM). Almonertinib mesylate is used for the research of the non-small cell lung cancer .

HY-150561

Trk-IN-20	Trk Receptor	Cancer
Trk-IN-20 is a kind of 3-vinylindazole derivatives. Trk-IN-20 suppresses Trk kinases functions by phosphorylation inhibition of TrkA/B/C with IC₅₀ values of 1.6 nM, 2.9 nM and 2.0 nM, respectively .

Cat. No.	Product Name

HY-L169

Anti-Drug-Resistant Compound Library	325 compounds
Resistance refers to the decrease in the effectiveness of drugs in treating diseases or symptoms. Due to the increasing global antibiotic resistance, it may threaten our ability to treat common infectious diseases. Drug resistance is also the main cause of chemotherapy failure in malignant tumors. In approximately 50% of cases, drug resistance exists even before chemotherapy begins. There are many mechanisms of anticancer drug resistance, including increased protein expression that leads to drug removal, mutations in drug binding sites, recovery of tumor protein production, and pre-existing genetic heterogeneity in tumor cell populations. In addition, the issue of drug resistance seems to have affected the development of new anticancer drugs. Drug resistance may be caused by various conditions, such as mutations, epigenetic modifications, and upregulation of drug efflux protein expression. Overcoming multidrug resistance in cancer treatment is becoming increasingly important. MCE designs a unique collection of 325 anti-drug-resistant compounds. It is a good tool to be used for research on cancer and other diseases.

Anti-Drug-Resistant Compound Library

325 compounds

Resistance refers to the decrease in the effectiveness of drugs in treating diseases or symptoms. Due to the increasing global antibiotic resistance, it may threaten our ability to treat common infectious diseases. Drug resistance is also the main cause of chemotherapy failure in malignant tumors. In approximately 50% of cases, drug resistance exists even before chemotherapy begins. There are many mechanisms of anticancer drug resistance, including increased protein expression that leads to drug removal, mutations in drug binding sites, recovery of tumor protein production, and pre-existing genetic heterogeneity in tumor cell populations. In addition, the issue of drug resistance seems to have affected the development of new anticancer drugs. Drug resistance may be caused by various conditions, such as mutations, epigenetic modifications, and upregulation of drug efflux protein expression. Overcoming multidrug resistance in cancer treatment is becoming increasingly important.

MCE designs a unique collection of 325 anti-drug-resistant compounds. It is a good tool to be used for research on cancer and other diseases.

HY-L129

Target Protein Ligand Library	39 compounds
Proteolysis-targeting chimera (PROTAC) has been developed to be a useful technology for targeted protein degradation. PROTACs consist of a ligand for E3 ligase (E3 ligase binder), a linker and a ligand (mostly small-molecule inhibitor) for protein of interest（target binder）. Upon binding to the target protein, the PROTACs can recruit E3 for target protein ubiquitination, which is subjected to proteasome-mediated degradation. Therefore, PROTACs execute their functions by degrading the target proteins rather than inhibiting them, which has a great superiority in overcoming resistance caused by target mutation or overexpression. To date, PROTAC technology has been applied to a variety of targets, including AR, ER, BTK, BET, and BCR-ABL to overcome resistance. MCE carefully prepared a unique collection of 39 ligands for target proteins, which have been reported to be used in PROTAC design. MCE Target Protein Ligand Library is a useful tool for PROTAC development.

Target Protein Ligand Library

39 compounds

Proteolysis-targeting chimera (PROTAC) has been developed to be a useful technology for targeted protein degradation. PROTACs consist of a ligand for E3 ligase (E3 ligase binder), a linker and a ligand (mostly small-molecule inhibitor) for protein of interest（target binder）. Upon binding to the target protein, the PROTACs can recruit E3 for target protein ubiquitination, which is subjected to proteasome-mediated degradation. Therefore, PROTACs execute their functions by degrading the target proteins rather than inhibiting them, which has a great superiority in overcoming resistance caused by target mutation or overexpression. To date, PROTAC technology has been applied to a variety of targets, including AR, ER, BTK, BET, and BCR-ABL to overcome resistance.

MCE carefully prepared a unique collection of 39 ligands for target proteins, which have been reported to be used in PROTAC design. MCE Target Protein Ligand Library is a useful tool for PROTAC development.

Dehydrojuncusol	Infection Structural Classification other families Classification of Application Fields Source classification Phenols Polyphenols Plants Disease Research Fields	HCV HCV Protease
Dehydrojuncusol, a potent HCV inhibitor, targets HCV NS5A and is able to inhibit RNA replication of replicons harboring resistance mutations to anti-NS5A direct-acting antivirals. Dehydrojuncusol significantly inhibits HCV infection when added after virus inoculation of HCV genotype 2a (EC₅₀=1.35 µM) .

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