Search Result

Results for "

chemotherapy resistance

" in MedChemExpress (MCE) Product Catalog:

By Targets:	BCRP (3) P-glycoprotein (5) Akt (2) AMPK (1) APC (1) Apoptosis (8) Autophagy (1) Biochemical Assay Reagents (1) c-Met/HGFR (1) Carbonic Anhydrase (1) Caspase (1) Checkpoint Kinase (Chk) (1) DNA-PK (3) DNA/RNA Synthesis (2) Endogenous Metabolite (2) Epigenetic Reader Domain (1) Glutathione Peroxidase (1) Heme Oxygenase (HO) (1) HIF/HIF Prolyl-Hydroxylase (1) Histone Methyltransferase (1) Itk (1) Ligands for Target Protein for PROTAC (1) MARK (1) MOFs (1) mRNA (1) mTOR (3) NF-κB (1) PI3K (1) Pim (1) PROTACs (1) Proton Pump (1) Reference Standards (2) Salt-inducible Kinase (SIK) (1) STAT (1) VEGFR (1)
By Research Areas:	Cancer (29) Cardiovascular Disease (1) Infection (1) Inflammation/Immunology (2) Metabolic Disease (1)
Oligonucleotides:	mRNA (1) Antisense Oligonucleotides (1)

Inhibitors & Agonists

Screening Libraries

Peptides

Oligonucleotides

GMP Molecules

Targets Recommended: BCRP P-glycoprotein

Cat. No.	상품명	Target	연구분야	Chemical Structure

HY-101570

Nedisertib Maximum Cited Publications 27 Publications Verification Peposertib; M3814	DNA-PK BCRP	Cancer
Nedisertib (Peposertib) is an orally active selective DNA-dependent protein kinase (DNA-PK) inhibitor with an IC₅₀ value of less than 3 nM. Nedisertib also acts as a modulator of ABCG2, capable of reversing ABCG2-mediated multidrug resistance (MDR), thus providing new strategies for combination therapy. By inhibiting DNA double-strand break repair, Nedisertib can enhance the efficacy of chemotherapy and radiotherapy. Nedisertib exhibits antitumor activity .

HY-107636

DC_AC50 5+ Cited Publications	Apoptosis	Cancer
DC_AC50 is a dual inhibitor of Atox1 and CCS (copper chaperones). Inhibiting intracellular copper chaperones as a means of reducing/preventing acquired chemotherapy resistance .

HY-120877

MRT199665	MARK Salt-inducible Kinase (SIK) AMPK Apoptosis	Cancer
MRT199665 is a potent and ATP-competitive, selective MARK/SIK/AMPK inhibitor with IC₅₀s of 2/2/3/2 nM, 10/10 nM, and 110/12/43 nM for MARK1/MARK2/MARK3/MARK14, AMPKα1/AMPKα2, and SIK1/SIK2/SIK3, respectively . MRT199665 causes apoptosis in MEF2C-activated human acute myeloid leukemias (AML) cells . MRT199665 inhibits the phosphorylation of SIK substrate CRTC3 at S370 .

HY-P2657

Verucopeptin	HIF/HIF Prolyl-Hydroxylase Proton Pump Endogenous Metabolite	Cancer
Verucopeptin is a potent HIF-1 (IC50=0.22 μM) inhibitor and decreases the expression of HIF-1 target genes and HIF-1α protein levels. Verucopeptin strongly inhibits v-ATPase activity by directly targeting the v-ATPase ATP6V1G subunit but not ATP1V1B2 or ATP6V1D. Verucopeptin exhibits antitumor activity against multidrug resistance (MDR) cancers and can be used for cancer research.

HY-119198

NSC745885	Apoptosis Histone Methyltransferase	Cancer
NSC745885 an effective anti-tumor agent, shows selective toxicity against multiple cancer cell lines but not normal cells. NSC745885 is an effective down-regulator of EZH2 via proteasome-mediated degradation. NSC745885 provides possibilities for the study of advanced bladder and oral squamous cell carcinoma (OSCC) cancers .

HY-P1823

C-Reactive Protein (CRP) (174-185)	Akt mTOR Caspase	Infection Cardiovascular Disease Metabolic Disease Inflammation/Immunology Cancer
C-Reactive Protein (CRP) is an anti-pneumococcal plasma protein that can serve as an inflammatory marker. C-Reactive protein can protect mice from pneumococcal infection by activating complement. C-Reactive protein can inhibit the activation of caspase-3/9 through the CD64/AKT/mTOR pathway, thereby promoting chemotherapy resistance in mice with tongue squamous cell carcinoma .

HY-130841

Apcin-A	APC Ligands for Target Protein for PROTAC	Cancer
Apcin-A is a small molecule inhibitor that selectively targets the cell division cycle protein Cdc20 and is a derivative of Apcin (HY-110287). Apcin-A competitively binds to the D-box binding pocket of Cdc20 and inhibits substrate ubiquitination mediated by the anaphase promoting complex APC/C-Cdc20. Apcin-A also blocks the binding of Cdc20 to substrates (such as securin and cyclin B1), inhibiting anaphase initiation and cell cycle exit. Apcin-A can promote or prolong mitotic slippage in coordination with p31 ^comet under conditions of high spindle assembly checkpoint (SAC) activity. Apcin-A can be used to develop anti-mitotic drugs and overcome tumor chemotherapy resistance. Apcin-A can be used to synthesize PROTAC CP5V (HY-130257)[1][2][3].

HY-155339

Anticancer agent 168	Apoptosis DNA/RNA Synthesis	Cancer
Anticancer agent 168 (compound d16) is a inhibitor of DNA2. Anticancer agent 168 induces apoptosis and cell-cycle arrest mainly at S-phase, and exhibits anticancer activities and overcomes chemotherapy resistance in mutp53-bearing cancers .

HY-157169

IBL-302 AMU302	Pim mTOR Akt PI3K	Cancer
IBL-302 (AMU302) is an orally available dual-signaling inhibitor of PIM and PI3K/AKT/mTOR with activity against breast cancer and neuroblastoma. IBL-302 demonstrated in vivo efficacy in a nude mouse xenograft model, inhibiting trastuzumab (HY-P9907) resistance challenges. IBL-302 also enhances the effects of common cytotoxic chemotherapy drugs cisplatin (HY-17394), doxorubicin (HY-15142A), and etoposide (HY-13629) .

HY-104067

Naphthol AS-MX phosphate NASTRp	Epigenetic Reader Domain	Cancer
Naphthol AS-MX phosphate (NASTRp) is a small molecule inhibitor of the CREB (cyclic adenosine phosphate reaction element binding protein)-CBP (CREB binding protein) transcription factor complex. Naphthol AS-MX phosphate shows antitumor activity against lung cancer cells, inhibiting tumor cell proliferation (IC₅₀=3.701 μmol/L), colony formation, and anchored independent growth in soft AGAR. Naphthol AS-MX phosphate can be used in the study of KRAS mutated lung cancer, especially for KRAS mutated lung cancer with poor chemotherapy resistance and prognosis .

HY-143230A

Custirsen sodium OGX-011 sodium	Apoptosis	Cancer
Custirsen sodium is a highly specific antisense oligonucleotide that inhibits the production of clusterin , an antiapoptotic protein that is upregulated in response to chemotherapy and that confers treatment resistance.

HY-176758

GPX4-IN-17	Glutathione Peroxidase	Cancer
GPX4-IN-17 (Compound 9i) is an inhibitor of GPX4 with potent cytotoxicity (IC₅₀ = 0.3 nM). GPX4-IN-17 shows strong binding affinity against GPX4 (K_D = 20.4 nM). GPX4-IN-17 inhibits tumor growth in the xenograft tumor mouse model without detectable cytotoxicity. GPX4-IN-17 can enhance cancer chemotherapy and overcome tumor resistance. GPX4-IN-17 can be studied in antitumor reseach .

HY-177551

CHK1-IN-14	Checkpoint Kinase (Chk)	Cancer
CHK1-IN-14 is a free base form of CHK1 inhibitor. CHK1-IN-14 can be used in research on resistance to chemotherapy and radiotherapy .

HY-124582

NEO214 1 Publications Verification	Autophagy mTOR	Cancer
NEO214 is an autophagy inhibitor and a covalent conjugate of the PDE4 inhibitor Rolipram (HY-16900) and perillyl alcohol (HY-N7000). It has anti-cancer activity and blood-brain barrier (BBB) permeability. Over sex. NEO214 prevents autophagy-lysosome fusion, thereby blocking autophagic flux and triggering glioma cell death. The process involves mTOR activation, andTFEB(Transcription Factor EB) aggregation. NEO214 inhibitionMacroautophagy/autophagy in glioblastoma cells has the potential to overcome chemotherapy resistance in glioblastoma .

HY-101570G

Nedisertib Peposertib; M3814	DNA-PK BCRP	Cancer
Nedisertib (GMP) (Peposertib (GMP)) is Nedisertib (HY-101570) produced by using GMP guidelines. GMP small molecules works appropriately as an auxiliary reagent for cell therapy manufacture. Nedisertib is an orally active selective DNA-dependent protein kinase (DNA-PK) inhibitor with an IC₅₀ value of less than 3 nM. Nedisertib also acts as a modulator of ABCG2, capable of reversing ABCG2-mediated multidrug resistance (MDR), thus providing new strategies for combination therapy. By inhibiting DNA double-strand break repair, Nedisertib can enhance the efficacy of chemotherapy and radiotherapy. Nedisertib exhibits antitumor activity .

HY-185206

BSJ-05-037	PROTACs Itk NF-κB	Cancer
BSJ-05-037 is an ITK PROTAC degrader that effectively targets and degrades ITK in T-cell lymphoma cell lines. BSJ-05-037 blocks the activation of the NF-κB/GATA-3 signaling pathway, inhibits PLCγ1 phosphorylation, and reduces the proliferative capacity of T-cell lymphoma cells. BSJ-05-037 enhances the sensitivity of T-cell lymphoma cells to chemotherapy. In mouse models of T-cell lymphoma, BSJ-05-037 induces ITK degradation, reduces GATA-3 expression, decreases tumor volume, and reverses chemotherapy resistance. BSJ-05-037 is applicable to research related to T-cell lymphoma .

HY-170837

STAT5-IN-3	STAT	Cancer
STAT5-IN-3 (Compound 14a) is a STAT5 inhibitor with anticancer activity. STAT5-IN-3 blocks the tyrosine phosphorylation of STAT5A/5B at the Y694/699 sites and significantly reduces the expression of STAT5B protein, thereby inhibiting downstream gene transcription and blocking the proliferation and survival of leukemia cells. Additionally, STAT5-IN-3 holds significant value in overcoming chemotherapy resistance .

HY-106753

Tolnapersine	P-glycoprotein	Others
Tolnapersine exhibits multidrug resistance (MDR) reversal activity, which reverses the resistance of tumor cells to multiple chemotherapy drugs by affecting P-glycoprotein (Pgp) on the cell membrane .

HY-163687

Tropirine BS-7723 free base	Biochemical Assay Reagents	Cancer
Tropirine (BS-7723 free base) is a radiosensitizer. Tropirine can be used in cancer research .

HY-161645

P-gp modulator-4	P-glycoprotein	Cancer
P-gp modulator-4 (compound 4c) inhibits the efflux function of P-glycoprotein (P-gp). P-gp modulator-4 shows multidrug resistance (MDR) in cancer reversal activity (IC₅₀ of Paclitaxel (HY-B0015) = 8.80, reversal fold = 211.8) .

HY-136476B

Cu(II) protoporphyrin IX	Heme Oxygenase (HO) MOFs	Inflammation/Immunology Cancer
Cu (II) Protoporphyrin IX is used as a negative control for Zn (II) Protoporphyrin (an inihibitor of heme oxygenase). Heme oxygenase has been implicated in tumor cell resistance to chemotherapy, reduction of free radical formation and inflammation, and associated with vascular repair .

HY-13574

Biricodar dicitrate VX 710-3	P-glycoprotein	Cancer
Biricodar dicitrate (VX 710-3) is the dicitrate salt form of Biricodar (HY-13574A). Biricodar dicitrate is an inhibitor for P-glycoprotein and multidrug resistance-associated protein 1 (MRP-1), which increases the accumulation of chemotherapy drugs within cancer cells and shows effective chemosensitizing activity in multidrug resistant cells .

HY-161623

ERCC1/XPA interaction inhibitor 1	DNA/RNA Synthesis	Cancer
ERCC1/XPA interaction inhibitor 1 (compound 27o) is a potent ERCC1/XPA67-80 interaction inhibitor with an EC₅₀ value of 4.7 µM. ERCC1/XPA interaction inhibitor 1 has the potential for the research of DNA damaging agents and overcoming resistance to platinum-based chemotherapy .

HY-E70298

ST3 β-Gal α-2,3-Sialyltransferase 1 ST3GAL1	Endogenous Metabolite	Cancer
ST3 β-Gal α-2,3-Sialyltransferase 1 (ST3GAL1) is a sialyltransferase whose overexpression in ovarian cancer cell lines enhances cell growth, migration, and invasion capabilities, as well as increases tumorigenicity and resistance to paclitaxel in vivo. ST3 β-Gal α-2,3-Sialyltransferase 1 catalyzes the transfer of sialic acid from cytidine monophosphate-sialic acid to galactose-containing substrates and can be utilized in studies of cancer progression and chemotherapy resistance .

HY-174324

VEGFR-2/P-gp-IN-1	VEGFR P-glycoprotein Apoptosis	Cancer
VEGFR-2/P-gp-IN-1, a Licochalcone A (HY-N0372) derivative, is an orally active VEGFR-2 (IC₅₀ = 0.885 μM) and P-gp inhibitor. VEGFR-2/P-gp-IN-1 achieves anti-tumor proliferation and overcomes chemotherapy resistance by synchronously inhibiting VEGFR-2 kinase activity and P-gp drug efflux pump function. VEGFR-2/P-gp-IN-1 inhibits phosphorylation of VEGFR-2 and downstream PI3K/AKT signaling pathway proteins, induces apoptosis, blocks cells in the S phase, and inhibits invasive migration. VEGFR-2/P-gp-IN-1 exerts potent in vivo anti-tumor effects in the HeLa/DDP cell xenograft tumor model. VEGFR-2/P-gp-IN-1 is used in cervical cancer research.

HY-107636R

DC_AC50 (Standard)	Reference Standards Apoptosis	Cancer
DC_AC50 (Standard) is the analytical standard of DC_AC50 (HY-107636). This product is intended for research and analytical applications. DC_AC50 is a dual inhibitor of Atox1 and CCS (copper chaperones). Inhibiting intracellular copper chaperones as a means of reducing/preventing acquired chemotherapy resistance .

HY-174717

Human ERAS mRNA	mRNA	Cancer
Human ERAS mRNA encodes the human ES cell expressed Ras (ERAS) protein, a constitutively active member of the small GTPase Ras protein family. ERAS may be involved in cancer and chemotherapy resistance.

HY-179683

MRP1-IN-2	P-glycoprotein	Cancer
MRP1-IN-2 (Compound 21) is a selective MRP1 inhibitor with a relatively weak inhibitory effect on P-gp. MRP1-IN-2 exhibits a strong accumulation effect of calcein, with its EC₅₀ value being 177 nM. MRP1-IN-2 enhances the activity of Doxorubicin (HY-15142A) on drug-resistant cells. MRP1-IN-2 can be used for the study of multidrug-resistant cancers .

HY-101570R

Nedisertib (Standard) Peposertib (Standard); M3814 (Standard)	DNA-PK Reference Standards BCRP	Cancer
Nedisertib (Standard) is the analytical standard of Nedisertib (HY-101570). This product is intended for research and analytical applications. Nedisertib (Peposertib) is an orally active selective DNA-dependent protein kinase (DNA-PK) inhibitor with an IC50 value of less than 3 nM. Nedisertib also acts as a modulator of ABCG2, capable of reversing ABCG2-mediated multidrug resistance (MDR), thus providing new strategies for combination therapy. By inhibiting DNA double-strand break repair, Nedisertib can enhance the efficacy of chemotherapy and radiotherapy. Nedisertib exhibits antitumor activity .

HY-179034

CAIX/XII-IN-16	Carbonic Anhydrase c-Met/HGFR Apoptosis	Cancer
CAIX/XII-IN-16 (Compound 5d) is a selective inhibitor of CA IX/XII and c-Met. CAIX/XII-IN-16‘s K_i values for hCA IX, hCA XII and CA I are 10.6, 31.8 and 2361 nM respectively, and its IC₅₀ value for c-Met is 0.49 μM. CAIX/XII-IN-16 exhibits significantly enhanced cytotoxicity against colon cancer cells under hypoxic conditions. CAIX/XII-IN-16 causes cell cycle arrest and induces apoptosis (apoptosis). CAIX/XII-IN-16 significantly enhances the efficacy of Oxaliplatin (HY-17371) and 5-Fluorouracil (HY-90006). CAIX/XII-IN-16 can be used for studies on chemotherapy resistance related to hypoxia .

Cat. No.	상품명

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.

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-L234

Nucleotide Metabolite Compound Library	82 compounds
Nucleotide metabolism is central to cancer aggressiveness, underpinning uncontrolled proliferation, chemotherapy resistance, immune evasion, and metastasis. It is transcriptionally regulated by oncogenes (e.g., MYC) and tumor suppressors (e.g., pRb). Nucleotide imbalance and nucleoside degradation further regulate cell state transitions, especially following replication stress. Additionally, secretion of nucleotides/nucleosides into the tumor microenvironment modulates immune responses and influences treatment efficacy. Therefore, nucleotide metabolites have roles in disease response and indication in cancer research, and can be utilized to develop cancer-related mechanisms and drugs. MCE can provide 82 metabolites produced by nucleotide metabolic pathways, which can be used for disease mechanism research and drug research.

Nucleotide Metabolite Compound Library

82 compounds

Nucleotide metabolism is central to cancer aggressiveness, underpinning uncontrolled proliferation, chemotherapy resistance, immune evasion, and metastasis. It is transcriptionally regulated by oncogenes (e.g., MYC) and tumor suppressors (e.g., pRb). Nucleotide imbalance and nucleoside degradation further regulate cell state transitions, especially following replication stress. Additionally, secretion of nucleotides/nucleosides into the tumor microenvironment modulates immune responses and influences treatment efficacy. Therefore, nucleotide metabolites have roles in disease response and indication in cancer research, and can be utilized to develop cancer-related mechanisms and drugs.

MCE can provide 82 metabolites produced by nucleotide metabolic pathways, which can be used for disease mechanism research and drug research.

HY-L173

Anti-Ovarian Cancer Compound Library	2,817 compounds
Ovarian cancer is the most common cause of death in female genital malignancies, with the highest mortality rate in female genital malignancies. It is characterized by difficulty in detection in the early stage of the disease, high recurrence rate and poor prognosis. In fact, ovarian cancer includes many pathologic types. It is usually divided into epithelial ovarian cancer, malignant germ cell tumors and sex cord stromal tumors, of which epithelial ovarian cancer is the most dominant form. Clinical treatment of ovarian cancer prioritizes surgery combined with paclitaxel chemotherapy. However, due to the spread and drug resistance of tumor cells, the recurrence of ovarian cancer is high. In this case, combined with traditional methods, the development of new therapeutic agents can help to improve the treatment effect of ovarian cancer. MCE designs a unique collection of 2,817 compounds with definite or potential anti-ovarian cancer activity, which mainly targeting the main targets of ovarian cancer such as PARP, ATM/ATR, VEGFR and HIF/HIF Prolyl-Hydroxylase, etc. It is an essential tool for development and research of anti-ovarian compounds.

Anti-Ovarian Cancer Compound Library

2,817 compounds

Ovarian cancer is the most common cause of death in female genital malignancies, with the highest mortality rate in female genital malignancies. It is characterized by difficulty in detection in the early stage of the disease, high recurrence rate and poor prognosis. In fact, ovarian cancer includes many pathologic types. It is usually divided into epithelial ovarian cancer, malignant germ cell tumors and sex cord stromal tumors, of which epithelial ovarian cancer is the most dominant form. Clinical treatment of ovarian cancer prioritizes surgery combined with paclitaxel chemotherapy. However, due to the spread and drug resistance of tumor cells, the recurrence of ovarian cancer is high. In this case, combined with traditional methods, the development of new therapeutic agents can help to improve the treatment effect of ovarian cancer.

MCE designs a unique collection of 2,817 compounds with definite or potential anti-ovarian cancer activity, which mainly targeting the main targets of ovarian cancer such as PARP, ATM/ATR, VEGFR and HIF/HIF Prolyl-Hydroxylase, etc. It is an essential tool for development and research of anti-ovarian compounds.

Cat. No.	상품명	Target	Research Area