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Results for "

resistance mutation

" in MedChemExpress (MCE) Product Catalog:

By Targets:	Acetyl-CoA Carboxylase (1) Akt (3) Aldose Reductase (1) AMPK (1) Anaplastic lymphoma kinase (ALK) (6) Androgen Receptor (2) Antibiotic (1) Apoptosis (12) ATP Synthase (1) Aurora Kinase (1) Autophagy (2) Bacterial (1) Bcl-2 Family (1) Bcr-Abl (9) Btk (6) c-Kit (2) c-Met/HGFR (4) Caspase (2) Checkpoint Kinase (Chk) (1) CRM1 (1) DNA/RNA Synthesis (2) Drug Isomer (1) EGFR (14) Endogenous Metabolite (2) Enterovirus (1) ERK (2) FGFR (6) Flavivirus (1) FLT3 (2) Fungal (1) G-quadruplex (1) HCV (2) HCV Protease (1) HDAC (1) HIV (4) HIV Protease (2) HSP (1) Ligands for Target Protein for PROTAC (1) Microtubule/Tubulin (1) Mitochondrial Metabolism (1) Molecular Glues (1) Mps1 (1) mTOR (1) NF-κB (1) Parasite (1) PARP (2) PI3K (1) Poly(ADP-ribose) Glycohydrolase (PARG) (1) PROTACs (6) Raf (1) Ras (2) Reference Standards (3) Reverse Transcriptase (1) ROS Kinase (1) SARS-CoV (1) SOS1 (1) Src (2) Thyroid Hormone Receptor (2) Trk Receptor (3) TRP Channel (1) VDAC (1) Virus Protease (1)
By Research Areas:	Cancer (72) Endocrinology (1) Infection (14) Inflammation/Immunology (4) Metabolic Disease (4) Neurological Disease (2)
Click Chemistry:	Alkynes (3)

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-16909

Leptomycin B 20+ 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-147250

Lirafugratinib 1 Publications Verification 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-111373

RapaLink-1 10+ 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-112823

Almonertinib 5+ Cited Publications 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-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-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-148811

Zurletrectinib ICP-723	c-Met/HGFR Trk Receptor	Cancer
Zurletrectinib is a brain-penetrant, orally active TRK inhibitor (TRKA IC₅₀ = 0.81 nM; TRKB IC₅₀ = 0.145 nM; TRKC IC₅₀ = 0.184 nM). Zurletrectinib exhibits stronger activity as a consequence of its augmented binding affinity for TRK kinases. Zurletrectinib exhibits higher activity against most TRK inhibitor resistance mutations (13 out of 18 mutations). Zurletrectinib can be used for the study of glioma .

HY-172262

WEHI-3773	VDAC Bcl-2 Family Apoptosis	Cancer
WEHI-3773 is a VDAC2 ligand and apoptosis modulator. WEHI-3773 directly binds to the β7-β10 region of VDAC2 and disrupts its interaction with BAX and BAK. WEHI-3773 regulates BAX-mediated apoptosis in BAK-deficient cells by modulating conformational activation of BAX, mitochondrial redistribution, and cytochrome c release. WEHI-3773 overcomes Venetoclax (HY-15531) resistance, resensitizes leukemia cells carrying BAX mutations to BH3 mimetics, and enables long-term clonogenic survival of BAK-deficient cells treated with BH3 mimetics. WEHI-3773 is applicable to research related to acute myeloid leukemia .

HY-136420

SJF-0628	PROTACs Raf Apoptosis	Inflammation/Immunology Cancer
SJF-0628 is a RAF PROTAC degrader. SJF-0628 induces targeted degradation of BRAF in various cancer cell lines (colorectal cancer cell lines (Colo-205, LS-411N, HT-29, RKO) and triple-negative breast cancer cell line DU-4475). SJF-0628 decreases pMEK and pErk levels in DU-4475 cells. SJF-0628 has anti-tumor activity. SJF-0628 can be used for research of colorectal cancer and triple-negative breast cancer. (Pink: RAF ligand (HY-12057), Blue: VHL Ligand ( HY-125845), Black: Linker (HY-B0912)) .

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-147250A

Lirafugratinib hydrochloride 1 Publications Verification 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-137849

RK-582	PARP	Cancer
RK-582 is a tankyrase inhibitor, antitumor agent, and orally bioavailable growth inhibitor, with an IC₅₀ of 36.1 nM against human tankyrase-1 and an IC₅₀ of 39.2 nM against human tankyrase-2. In APC-mutated colorectal cancer cells, the sensitivity to RK-582 correlates with the level of active β-catenin, while drug resistance associates with PIK3CA mutation. RK-582 can be used for the research of colorectal cancer .

HY-153268

Silevertinib 2 Publications Verification BDTX-1535; EGFR-IN-76	EGFR	Infection Neurological Disease Metabolic Disease Cancer
Silevertinib (BDTX-1535) is an irreversible, brain-penetrant, selective and orally active EGFR inhibitor with wild-type EGFR-sparing. Silevertinib targets key EGFR resistance mutations, including the kinase domain (C797S, L718Q, G724S, S768I), extracellular domain (EGFRvIII, A289X), and EGFR amplification. Silevertinib exerts anti-tumor activity with well tolerated in vivo. Silevertinib can be used for non-small cell lung cancer (NSCLC) and glioblastoma (GBM) research .

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-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-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-112823A

Almonertinib mesylate 5+ Cited Publications 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-112823B

Almonertinib hydrochloride 5+ Cited Publications 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-175839

PROTAC EGFR degrader 15	PROTACs EGFR ATP Synthase	Cancer
PROTAC EGFR degrader 15 is a Pomalidomide (HY-10984)-based Gefitinib (HY-50895) EGFR PROTAC degrader. PROTAC EGFR degrader 15 triggers EGFR degradation via ubiquitin-proteasome-dependent proteolysis and autophagy-lysosome activation pathways. PROTAC EGFR degrader 15 targets ETFA to enhance ATP production. PROTAC EGFR degrader 15 significantly suppresses tumor growth in a Gefitinib-acquired resistant HCC-827 xenograft model. PROTAC EGFR degrader 15 can be used for the study of non-small cell lung cancer (NSCLC) (Pink: EGFR ligand (HY-W109039); Blue: CRBN ligand (HY-10984); Black: Linker (HY-W679737)) .

HY-160167

Birelentinib DZD8586	Src Btk	Inflammation/Immunology Cancer
Birelentinib (DZD8586) is an orally effective, selective, non-covalent inhibitor targeting LYN tyrosine kinase and BTK tyrosine kinase, capable of penetrating the blood-brain barrier. Birelentinib exhibits concentration-dependent antiproliferative effects in RI-1 cells and diffuse large B-cell lymphoma (DLBCL) cell lines carrying BTK resistance mutations (such as C481X, V416L, etc.). Birelentinib blocks both BTK-dependent and independent signaling of the B-cell receptor (BCR), thereby inhibiting tumor cell proliferation and inducing cell death. Birelentinib can be used in research to overcome resistance to existing covalent and non-covalent BTK inhibitors in B-cell non-Hodgkin lymphoma (B-NHL) .

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-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-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-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-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-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-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-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-164548

WK88-1	HSP Apoptosis PI3K Akt NF-κB	Inflammation/Immunology Cancer
WK88-1 is an apoptosis inducer and Hsp90 client protein inhibitor with antiproliferative and immunomodulatory activities. WK88-1 inhibits signaling pathways such as PI3K/Akt and NF-κB, and induces mitochondrial dysfunction and cell cycle arrest. WK88-1 effectively suppresses cancer cell migration and invasion, and reverses various EGFR mutations and resistance to Gefitinib (HY-50895). WK88-1 also regulates the differentiation of monocytes and dendritic cells, blocks the expression of multiple chemokines, inhibits immune cell migration and M1 marker transcription, and restores impaired endocytic activity. WK88-1 has been used in studies of breast cancer, non-small cell lung cancer with various EGFR mutations or Met amplification, and atherosclerosis and other related diseases .

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-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-179403

KRASG12C IN-17	Ras	Cancer
KRASG12C IN-17 is an orally active covalent KRAS ^G12C inhibitor, showing strong inhibitory activity in KRAS ^G12C-mutant cancer cells (NCI-H23 IC₅₀ = 0.7 nM; NCI-H358 IC₅₀ = 0.5 nM). KRASG12C IN-17 covalently and irreversibly binds to KRAS ^G12C with > 96% modification efficiency in both GDP-bound and GMPPNP-bound conformations. KRASG12C IN-17 can be used for studies of KRAS-driven cancers, including colorectal cancer .

HY-E70634

ABL1 E255K Recombinant Human Active Protein Kinase	Bcr-Abl	Cancer
The emergence of mutations in the BCR::ABL1 kinase domain (KD) impairs Imatinib Mesylate (HY-50946) binding capacity, thus contributing to Imatinib Mesylate resistance. Identification of these mutations is important for treatment decisions and precision medicine in chronic myeloid leukaemia (CML). ABL1 E255K Recombinant Human Active Protein Kinase is a recombinant ABL1 E255K protein that can be used to study ABL1 E255K-related functions .

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-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-115443

MZH29	FLT3	Cancer
MZH29 is a potent and orally active FLT3 inhibitor. MZH29 shows inhibitory effects on wild-type and mutant FLT3, including the FLT3-ITD, FLT3-D835H/Y/V and FLT3-K663Q mutants. MZH29 retains its potent inhibitory effect against the FLT3-ITD/F691L mutation, a drug resistance mutation against the well-known FLT3 inhibitor, AC220 (HY-13001). MZH29 can be used for the research of cancer, such as acute myeloid leukemia (AML) .

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-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-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-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-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-105369

KF-20444	Anaplastic lymphoma kinase (ALK) Apoptosis	Cancer
KF-20444 is an orally active ALK inhibitor with blood-brain barrier penetration. KF-20444 exhibits strong inhibitory activity against ALK fusion proteins (EML4-ALK) and ALK resistance mutations (including L1196M, G1202R, and F1174L). KF-20444 effectively suppresses the phosphorylation of ALK in ALK-driven cancer cell lines, thereby inhibiting cancer cell proliferation and inducing apoptosis. KF-20444 demonstrates anti-tumor efficacy in mouse models bearing ALK-positive non-small cell lung cancer (NSCLC) or neuroblastoma. KF-20444 can be used for the study of ALK-driven malignancies .

HY-153321A

(R,R)-Bexobrutideg (R,R)-NX-5948; (R,R)-BTK-IN-24	Drug Isomer PROTACs Btk	Inflammation/Immunology Cancer
(R,R)-Bexobrutideg is the (R,R)-enantiomer of Bexobrutideg (HY-153321). Bexobrutideg (NX-5948) is an orally active PROTAC that induces specific BTK protein degradation via a cereblon E3 ligase (CRBN) complex without degrading other cereblon neo substrates. Bexobrutideg mediates potent anti-inflammatory activity through BTK degradation, thereby inhibiting B cell activation. Bexobrutideg exhibits potent tumor growth inhibition in TMD8 xenograft models containing wild-type BTK or BTKi resistance mutations. Bexobrutideg is effective in a mouse model of collagen-induced arthritis (CIA). Bexobrutideg can cross the blood-brain barrier. NX-5948 consists of a target protein ligand, a linker, and a VHL E3 ubiquitin ligase (Red: BTK ligand (HY-170324); Blue: CRBN ligand (HY-171893); Black: linker) .

HY-178938

AR Degrader-3	Molecular Glues Androgen Receptor Caspase Apoptosis	Endocrinology Cancer
AR Degrader-3 is an orally active molecular glue that targets AR/ARV7 and induces the degradation of AR and ARV7 through the ubiquitin-proteasome pathway (UPP). AR Degrader-3 directly interacts with the ligand-binding domain (LBD) and the N-terminal domain (NTD) of AR. AR Degrader-3 effectively suppresses the transcriptional activity of wild-type AR (AR-WT), AR mutants, and ARV7. AR Degrader-3 downregulates the mRNA and protein levels of downstream AR target genes, thereby overcoming antiandrogen resistance mediated by ARV7 and AR point mutations. AR Degrader-3 induces apoptosis in Enzalutamide (HY-70002) (ENZa)-resistant cells and increases cleaved caspase-3 protein levels. AR Degrader-3 can be used for the study of castration-resistant prostate cancer (CRPC) .

HY-179562

BTK degrader-2	Btk	Cancer
BTK degrader-2 (Example 2) is a BTK dual-functional degrading agent, which causes the degradation of BTK through the ubiquitin-proteasome pathway. BTK degrader-2 can be used for the study of B-cell-related diseases .

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-E70828

FGFR3 V555L Recombinant Human Active Protein Kinase	FGFR	Cancer
FGFR3 kinase mutations are associated with a variety of malignancies. FGFR3 V555L mutation leads to resistance to FGFR inhibitors. FGFR3 V555L Recombinant Human Active Protein Kinase is a recombinant FGFR3 V555L protein that can be used to study FGFR3 V555L-related functions .

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-E70829

FGFR3 V555M Recombinant Human Active Protein Kinase	FGFR	Cancer
FGFR3 kinase mutations are associated with a variety of malignancies. FGFR3 V555M mutation leads to resistance to FGFR inhibitors. FGFR3 V555M Recombinant Human Active Protein Kinase is a recombinant FGFR3 V555M protein that can be used to study FGFR3 V555M-related functions .

Cat. No.	Product Name

HY-L169

Anti-Drug-Resistant Compound Library

639 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 639 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

94 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 94 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.

HY-L940

Antiviral Lead-like compound library

5,813 compounds

Owing to the widespread transmission and frequent mutation of viral diseases, as well as the continuous emergence of new viruses and drug-resistant strains, antiviral drug development is facing increasingly stringent requirements. Antiviral compound libraries serve as important tools for drug screening, mechanism research and development, enabling the discovery and investigation of various antiviral drugs.

These compounds act through diverse antiviral mechanisms, targeting key steps in viral replication, assembly and invasion. They exert antiviral effects by inhibiting viral nucleic acid synthesis, blocking viral protein processing, and preventing viral binding to host cells. This library covers various types of antiviral compounds, including nucleosides, non-nucleosides, protease inhibitors and integrase inhibitors. It supports research on influenza virus, herpes virus, hepatitis virus, emerging respiratory viruses and other pathogens, and enables high-throughput screening of novel antiviral candidates to rapidly identify potential active compounds against diverse viruses. It also facilitates mechanistic studies to elucidate drug-target interactions and viral resistance mechanisms, and supports the screening of effective compounds against mutant strains for research on viral variation and drug resistance.

This antiviral library consists of 6,804 compounds with lead-like physicochemical properties. The core sources of the compounds include analogs of known antiviral molecues with a similarity score ≥ 0.6. MCE has collected more than 1450 antiviral molecules. As a small-molecule collection with both activity potential and structural modifiability, it provides strong support for antiviral drug research and development.

Cat. No.	Product Name	Target	Research Area	Image

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 .

Cat. No.	Product Name	Category	Target	Chemical Structure

HY-N12109

Albizziin	Microorganisms Ketones, Aldehydes, Acids Source Classification	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-N8188

Dehydrojuncusol	Infection other families Classification of Application Fields Phenols Polyphenols Plants Disease Research Fields Source Classification	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) .

Cat. No.	Product Name		Classification

HY-179403

KRASG12C IN-17		Alkynes
KRASG12C IN-17 is an orally active covalent KRAS ^G12C inhibitor, showing strong inhibitory activity in KRAS ^G12C-mutant cancer cells (NCI-H23 IC₅₀ = 0.7 nM; NCI-H358 IC₅₀ = 0.5 nM). KRASG12C IN-17 covalently and irreversibly binds to KRAS ^G12C with > 96% modification efficiency in both GDP-bound and GMPPNP-bound conformations. KRASG12C IN-17 can be used for studies of KRAS-driven cancers, including colorectal cancer .

HY-167690

MK-6186		Alkynes
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-179404

KRASG12C IN-18		Alkynes
KRASG12C IN-18 is an orally active covalent KRAS ^G12C inhibitor that achieves complete covalent engagement of KRAS ^G12C in both GDP- and GMPPNP-bound states and displays strong antiproliferative activity against KRAS ^G12C and resistance-associated variants, including KRAS ^G12C/R68S, with low-nanomolar IC₅₀ values. KRASG12C IN-18 exhibits marked in vivo efficacy in KRAS ^G12C-driven solid tumor and KRAS ^G12C/R68S xenograft models and can be used for colorectal cancer research .

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