Search Result

Results for "

resistance mutations

" in MedChemExpress (MCE) Product Catalog:

By Targets:	Acetyl-CoA Carboxylase (1) Akt (1) AMPK (1) Anaplastic lymphoma kinase (ALK) (5) Androgen Receptor (1) Antibiotic (1) Apoptosis (3) Aurora Kinase (1) Autophagy (2) Bacterial (1) Btk (1) c-Met/HGFR (3) Checkpoint Kinase (Chk) (1) CRM1 (1) DNA/RNA Synthesis (1) EGFR (10) Endogenous Metabolite (2) ERK (1) FGFR (2) Flavivirus (1) FLT3 (1) Fungal (1) G-quadruplex (1) GABA Receptor (1) HCV (2) HCV Protease (1) HDAC (1) HIV (2) Ligands for Target Protein for PROTAC (1) Mitochondrial Metabolism (1) Mps1 (1) mTOR (1) PARP (1) Poly(ADP-ribose) Glycohydrolase (PARG) (1) PROTACs (1) Reference Standards (1) Reverse Transcriptase (1) ROS Kinase (1) Thyroid Hormone Receptor (2) Trk Receptor (1)
By Research Areas:	Cancer (33) Infection (7) Metabolic Disease (2)
Click Chemistry:	Alkynes (1)

Inhibitors & Agonists

Screening Libraries

Inhibitory Antibodies

Natural
Products

Click Chemistry

Targets Recommended: BCRP P-glycoprotein

Cat. No.	Product Name	Target	Research Areas	Chemical Structure

HY-152292

Zidesamtinib NVL-520; NUV-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-N12109

Albizziin	Others	Others
Albizziin is an amino acid analog with activity as a competitive inhibitor of asparagine synthetase. Albizziin has been used to isolate Chinese hamster ovary cell mutants with altered levels of the target enzyme. Several mutational classes of albizziin can be distinguished based on cross-resistance to β-aspartic hydroxamic acid. Studies on asparagine synthetase have shown that resistance to albizziin may be associated with altered regulation of asparagine synthetase, structural mutations of the enzyme, and gene amplification .

HY-19815

Olafertinib CK-101; RX518	EGFR	Cancer
Olafertinib (CK-101) is an orally available, third generation and irreversible epidermal growth factor receptor tyrosine kinase inhibitor (EGFR-TKI). Olafertinib selectively inhibits both EGFR-TKI-sensitizing and resistance mutations with minimal activity on wild-type EGFR. Olafertinib can be used in research for non-small cell lung cancer (NSCLC) with EGFR mutations and other advanced malignancies .

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-164516

ONCOII	Mps1	Cancer
ONCOII is an Mps1 inhibitor with an IC₅₀ of 10.8 nM. The inhibitory activity of ONCOII against Mps1 is affected by naturally occurring mutations in the Mps1 gene, and cells with Mps1 mutations exhibit increased resistance to ONCOII. ONCOII can be used in cancer research .

HY-B0013

Lavofloxacin lactate (-)-Ofloxacin lactate	Bacterial DNA/RNA Synthesis	Infection
Lavofloxacin lactate ((-)-ofloxacin lactate) is a class of broad-spectrum antimicrobials that can kill or inhibit a variety of bacteria. Lavofloxacin lactate binds to DNA rotase and topoisomerase IV, resulting in blocked DNA replication and repair, thus inhibiting bacterial growth. Lavofloxacin lactate can be used to study resistance mechanisms in bacteria, including studying resistance genes and mutations .

HY-174387

KIN-8741	c-Met/HGFR	Cancer
KIN-8741 is a highly selective Type IIb c-Met inhibitor. KIN-8741 has broad activity against c-Met kinase mutations. KIN-8741 shows antitumor activity in MET gene amplified and exon 14 deleted non-small cell lung cancer models. KIN-8741 can be used in the research of c-Met driven cancers, especially advanced tumors carrying MET exon 14 jump mutations, acquired drug resistance mutations, etc .

HY-123649

MK-4882	HCV	Others
MK-4882 is an HCV NS5A inhibitor with activity in reducing viral load in a chimpanzee model of HCV infection, but with issues of viral breakthrough, prompting the development of compounds with greater potency against more genotypes and NS5A resistance mutations.

HY-164464

BPI-15086	EGFR	Cancer
BPI-15086 an orally active, potent, irreversible mutant-selective inhibitor of both EGFR and *T790M resistance* mutations tyrosine kinase**. BPI-15086 can be used for the research of non-small-cell lung cancer .

HY-167948

Dacomitinib metabolite M1/2	EGFR	Cancer
Dacomitinib metabolite M1/2 is a potent inhibitor of both wild-type (WT) EGFR and the T790M mutation, demonstrating significant activity against acquired resistance mechanisms in EGFR-mutant non-small-cell lung cancer (NSCLC).

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-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-158185

Isocycloseram	GABA Receptor	Others
Isocycloseram is an isoxazoline insecticide and acaricide widely recognized as an allosteric modulator of GABA-gated chloride channels. Isocycloseram is active against Lepidopteran, Hemiptera, Coleoptera, Thysanoptera and Diptera pests. Isocycloseram targets the invertebrate Rdl GABA receptor, but the G335M mutation in the third transmembrane domain of the Rdl GABA receptor may mediate resistance .

HY-109189

Rezivertinib 1 Publications Verification 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-153857

Lasmotinib PHI-101	FLT3 Checkpoint Kinase (Chk)	Cancer
Lasmotinib (PHI-101) is a FLT3 and CHK2 inhibitor. Lasmotinib 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. Lasmotinib synergizes with Venetoclax (HY-15531) or Azacytidine to inhibit leukemia. Lasmotinib exhibits anticancer activity against ovarian and breast cancer .

HY-174314

WZH-15-125	Ligands for Target Protein for PROTAC Anaplastic lymphoma kinase (ALK)	Cancer
WZH-15-125 is a potent ALK inhibitor. WZH-15-125 can effectively overcome drug resistance, especially compound ALK mutations. WZH-15-125 has an IC₅₀ of 101.7 nM for the highly refractory G1202R/L1196M mutation that is resistant to Lorlatinib (HY-12215). WZH-15-125 can be used as a PROTAC target protein ligand to synthesize PROTAC WZH-17-002 (HY-174315). WZH-15-125 can be used in the research of non-small cell lung cancer .

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-111373

RapaLink-1 5+ Cited Publications	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-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-P991572

MM-151	EGFR	Cancer
MM-151 is a humanized IgG1 monoclonal antibody targeting EGFR. MM-151 binds multiple regions of the EGFR extracellular domain (ECD) and reduces its mutations in circulating cell-free tumor DNA with EGFR resistance. MM-151 significantly inhibits EGFR signaling and cell growth. MM-151 can be used for drug-resistant cancers research, such as colorectal, non-small cell lung and triple negative breast cancer .

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-W814315

Alectinib analog CH5424802 analog; RO5424802 analog; RG7853 analog	Anaplastic lymphoma kinase (ALK)	Cancer
Alectinib analog (CH5424802 analog) is a selective ALK inhibitor with activity in blocking resistance gating mutations. The synthetic optimization of alectinib analog allows it to be combined with specific peptides to improve the ability to target cancer cells. Alectinib analog exhibits low micromolar IC50 values in antiproliferation and shows good cytotoxic effects. The inhibitory activity of alectinib analog is closely related to its stability and release of active ingredients. Alectinib analog demonstrated the ability to inhibit vascular septal length or width in an in vivo zebrafish model .

HY-174303

NNRT-IN-9	HIV Reverse Transcriptase	Infection
NNRT-IN-9 (Compound EG28) is a non-nucleoside reverse transcriptase (NNRT) inhibitor. NNRT-IN-9 has potent antiviral and anti-resistance activity against wild-type (WT) HIV-1 and various clinically relevant mutations (E138K and K103N + Y181C) with EC₅₀s of 55, 67 and 3910 nM, respectively. NNRT-IN-9 can be used for acquired immune deficiency syndrome (AIDS) research .

HY-167710

CRCD2	Endogenous Metabolite	Cancer
CRCD2 is a small molecule NT5C2 nucleotidase inhibitor with enhanced 6-mercaptopurine cytotoxic activity. CRCD2 can effectively reverse 6-mercaptopurine resistance caused by mutations in the NT5C2 gene or non-genetic activation mechanisms. CRCD2 combined with 6-mercaptopurine can enhance its cytotoxic activity in NT5C2 wild-type leukemia, showing its potential in the treatment of acute lymphoblastic leukemia .

HY-174887

THR-β agonist 9	Thyroid Hormone Receptor AMPK Acetyl-CoA Carboxylase Mitochondrial Metabolism	Metabolic Disease
THR-β agonist 9 is a potent, selective, and His435 mutation-sensitive THR-β (EC₅₀: 3.2 nM) agonist. THR-β agonist 9 has moderate selectivity (approximately 10-fold) and good activation capacity (EC₅₀: 134.2 nM to 515.5 nM) for multiple His435 mutants (H435A, H435Y, and H435R). THR-β agonist 9 has the potential to be used in the study of dyslipidemia, metabolic dysfunction-associated steatohepatitis (MASH), or resistance to thyroid hormone (RTH) .

HY-167690

MK-6186	Endogenous Metabolite	Infection
MK-6186 is a novel non-nucleoside reverse transcriptase inhibitor with sub-nanomolar activity against wild-type viruses and the two most common NNRTI-resistant RT mutants (K103N and Y181C). MK-6186 exhibits excellent antiviral activity against K103N and Y181C mutant viruses. When MK-6186 targets 12 common NNRTI-associated mutant viruses, only two relatively rare mutants (Y188L and V106I/Y188L) show high resistance, with FC values exceeding 100, while the FC values of the remaining viruses are all below 10. In addition, when MK-6186 faces 96 clinical virus isolates carrying NNRTI-resistant mutations, most (70%) viruses show more than 10-fold resistance to efavirenz (EFV), while only 29% of mutant viruses show more than 10-fold resistance to MK-6186 .

HY-112823A

Almonertinib mesylate 5 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-112823

Almonertinib 5 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-112823B

Almonertinib hydrochloride 5 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-174850

CFON-026	Btk	Cancer
CFON-026 is a selective, orally active and non-covalent BTK inhibitor with an IC₅₀ of 0.27  nM. CFON-026 has significant antitumor activity against wild-type BTK (TMD8 and REC-1) and all clinically relevant BTK resistance mutations (BTK C481S, T474I, L528W and V416L). CFON-026 induces complete tumor regression in TMD8 xenograft mice model. CFON-026 can be used for research of hematological cancers like chronic lymphocytic leukemia and waldenström macroglobulinemia .

HY-174384

MET Transcription-IN-1	c-Met/HGFR Apoptosis G-quadruplex	Cancer
MET Transcription-IN-1 (Compound C3) is an orally active MET transcription inhibitor. MET Transcription-IN-1 can efficiently bind and stabilize the G-quadruplex in the MET promoter region, thereby inhibiting c-Met expression. MET Transcription-IN-1 can also overcome drug resistance caused by specific c-Met mutations. MET Transcription-IN-1 is capable of inhibiting tumor cell proliferation, migration, and invasion, as well as inducing cell cycle arrest and apoptosis. MET Transcription-IN-1 has antitumor activity, and can be used in the research of tumors such as non-small cell lung cancer .

HY-112823R

Almonertinib (Standard) HS-10296 (Standard)	Reference Standards EGFR	Cancer
Almonertinib (Standard) is the analytical standard of Almonertinib. This product is intended for research and analytical applications. 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-133531

PDD00017272	Poly(ADP-ribose) Glycohydrolase (PARG)	Cancer
PDD00017272 is an inhibitor of poly(ADP-ribose) glycohydrolase (PARG) (EC₅₀=4.8 nM) and an activator of PARP1/2. PDD00017272 inhibits its activity of hydrolyzing poly(ADP-ribose) (pADPr), resulting in the accumulation of pADPr on chromatin, interfering with DNA damage repair and replication processes, and inducing PARP1/2-dependent cytotoxicity. PDD00017272 can be used in cancer models with DNA repair defects (such as BRCA mutations) or resistance to PARP inhibitors. PDD00017272 has a PARG expression level-correlated inhibitory potency with EC₅₀ of 9.2 nM (PARG cells), the tumor cells with lower PARG expression are more sensitive .

HY-174315

WZH-17-002	PROTACs Anaplastic lymphoma kinase (ALK) Akt ERK	Cancer
WZH-17-002 is a WZH-15-125-based ALK PROTAC degrader with a DC₅₀ of 25 nM. WZH-17-002 enhances activities against Lorlatinib (HY-12215)-resistant ALK compound mutations. WZH-17-002 significantly reduces drug resistance in ALK-fusion non-small cell lung cancer (NSCLC) and inhibits tumor growth in EML4-ALK G1202R/L1196 M xenograft mice model . Pink: ALK ligand (HY-174314); Blue: CRBN ligase ligand (HY-14658); Black: linker (HY-174316)

HY-147245

Basroparib STP1002	PARP	Cancer
Basroparib (STP1002) is a selective, orally active inhibitor of tankyrase (TNKS1/TNKS2) with IC₅₀ of 29.94 nM and 3.68 nM for TNKS1 and TNKS2, respectively. Basroparib has an IC₅₀ of >10 μM for PARP1. Basroparib binds to TNKS, stabilizes AXIN1/2 proteins, blocks Wnt/β-catenin signaling pathway, inhibits tumor cell proliferation and induces apoptosis, while reducing cancer stem cell properties. Basroparib can be used in colorectal cancer (CRC) studies with KRAS mutations (such as G12V/G12D) to overcome acquired resistance to MEK inhibitors. STP1002 has synergistic antitumor activity with MEK inhibitors .

HY-153358

TNG260	HDAC	Cancer
TNG260 is a selective, orally effective inhibitor of HDAC1 and CoREST complex, with a 10-fold selectivity for HDAC1 over HDAC3 and a 500-fold selectivity for CoREST complex over NuRD and Sin3 complex. TNG260 reshapes the tumor immune microenvironment, reduces immunosuppressive neutrophil infiltration, promotes effector T cell recruitment, and reverses anti-PD-1 resistance caused by STK11 deficiency by inhibiting the activity of the CoREST-HDAC1 complex. TNG260 induces durable tumor regression in combination with α-PD1 in MC38 tumor-bearing mice with STK11 mutations, and has lower toxicity to bone marrow cells than non-selective HDAC inhibitors .

HY-16909

Leptomycin B 10+ Cited Publications CI 940; LMB	CRM1 Fungal Antibiotic	Infection Cancer
Leptomycin B (CI 940; LMB) is a potent inhibitor of the nuclear export of proteins. Leptomycin B inactivates CRM1/exportin 1 by covalent modification at a cysteine residue. Leptomycin B is a potent antifungal antibiotic blocking the eukaryotic cell cycle .

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 .

HY-164552

ZNU-IMB-Z15	Apoptosis Androgen Receptor	Cancer
ZNU-IMB-Z15 (Compound Z15) is an antagonist of the androgen receptor (AR) and also a selective degrader of AR and ARV7. ZNU-IMB-Z15 can directly bind to the ligand-binding domain (LBD) and activation function-1 region of AR, and promote AR degradation through the proteasome pathway. ZNU-IMB-Z15 effectively inhibits the transcriptional activity of AR, AR mutants, and AR splice variants (ARVs), downregulating the mRNA and protein levels of AR downstream target genes, thereby overcoming the resistance to second-generation antiandrogen drugs induced by AR LBD mutations, AR amplification, and ARVs in castration-resistant prostate cancer (CRPC). ZNU-IMB-Z15 can inhibit the proliferation of AR-positive CRPC cell lines and induce their apoptosis, demonstrating anticancer activity both in vivo and in vitro .

HY-122058

KRH-3955	HIV	Infection
KRH-3955 is a CXCR4 antagonist with good bioavailability and potent anti-HIV-1 activity. KRH-3955 can effectively inhibit the replication of X4 HIV-1, including clinical isolates from different donors. KRH-3955 also shows activity against recombinant X4 HIV-1 containing reverse transcriptase, protease and tyrosinase resistance mutations. KRH-3955 can inhibit the binding of SDF-1alpha to CXCR4 and calcium ion signaling through this receptor. KRH-3955 inhibits the binding of an antibody against CXCR4 to CXCR4, showing a potent antagonistic effect on CXCR4. KRH-3955 shows an oral bioavailability of 25.6% in rats and can inhibit the replication of X4 HIV-1 in vivo .

Cat. No.	Product Name

HY-L169

Anti-Drug-Resistant Compound Library	505 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 505 anti-drug-resistant compounds. It is a good tool to be used for research on cancer and other diseases.

Anti-Drug-Resistant Compound Library

505 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 505 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

60 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 60 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.

Cat. No.	Product Name	Target	Research Area