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Results for "

therapy resistance

" in MedChemExpress (MCE) Product Catalog:

By Targets:	BCRP (1) Akt (1) Apoptosis (3) Caspase (2) Cytochrome P450 (1) DNA-PK (1) Epigenetic Reader Domain (1) ERK (1) FAK (1) FGFR (1) HIF/HIF Prolyl-Hydroxylase (1) HIV (1) MicroRNA (1) Microtubule/Tubulin (1) p38 MAPK (2) PERK (1) Potassium Channel (1) PPAR (1) PROTACs (1) Ras (2) Reactive Oxygen Species (ROS) (1) Reverse Transcriptase (1) STAT (1) TNF Receptor (2)
By Research Areas:	Cancer (9) Infection (1)
Click Chemistry:	Alkynes (1)

Inhibitors & Agonists

Screening Libraries

Isotope-Labeled Compounds

Click Chemistry

Targets Recommended: BCRP P-glycoprotein

Cat. No.	Product Name	Target	Research Areas	Chemical Structure

HY-101570

Nedisertib 20+ Cited Publications 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-171281

Human microRNA 200c MIR200C	MicroRNA	Cancer
Human microRNA 200c (MIR200C), a nucleotide small endogenous non-coding RNA, is an illustrious tumor suppressor. Human microRNA 200c is one of the highly studied miRNAs in terms of development, stemness, proliferation, epithelial-mesenchymal transition (EMT), therapy resistance, and metastasis .

HY-106072

Vinzolidine LY 104208	Microtubule/Tubulin	Cancer
Vinzolidine is a semisynthetic derivative of the catharanthus alkaloid. Vinzolidine exerts its cytotoxic effect on tumor cells by interfering with microtubulin polymerization, thereby inhibiting cell division. Vinzolidine can be utilized in research to investigate synergistic effects when combined with other chemotherapeutic agents or biologic therapies, as well as to study cancer cells' tolerance or resistance to these treatments, and to explore approaches to overcome such obstacles .

HY-172922

FGFR-IN-19	FGFR	Cancer
Arg-IN-1 is a selective Arginine (Arg)-targeting covalent inhibitor with IC₅₀s of 9.7 nM and 30.4 nM for FGFR2 and FGFR3,respectively. Arg-IN-1 has the potential to avoid FGFR1/4-targeted toxicity as well as conquer acquired on-target resistance, potential for FGFR-targeting cancer therapy .

HY-174417

NNRT-IN-10	Reverse Transcriptase HIV Potassium Channel Cytochrome P450	Infection
NNRT-IN-10 is a potent, selective and orally active non-nucleoside HIV-1 reverse transcriptase (NNRTI) inhibitor with with an EC₅₀ values ranging from 1.16 to 18.3 nM for HIV and its mutant strains. NNRT-IN-10 exhibits good pharmacokinetic properties and favorable safety profiles. NNRT-IN-10 can be used for the study of AIDS, caused by HIV-1 .

HY-13766

Timcodar VX-853	PPAR	Others
Timcodar is a macrolide agent, and studies have shown that during adipogenesis, timcodar can significantly inhibit fat accumulation, with an effect similar to that of rapamycin. However, unlike rapamycin, timcodar does not cause immunosuppression and glucose resistance. In addition, timcodar can effectively inhibit the adipogenic transcriptional regulators PPAR?? and C/EBP??, thereby inhibiting genes involved in fat accumulation. These studies lay the foundation for timcodar as a potential anti-obesity therapy, as obesity is becoming a global epidemic.

HY-164473

DETD-35	ERK Akt STAT Apoptosis	Cancer
DETD-35 is an inhibitor of the MEK-ERK, Akt, and STAT3 signaling pathways, which promotes cancer cell apoptosis (Apoptosis) and reduces cancer cell resistance to Vemurafenib (HY-12057). The IC₅₀ values of DETD-35 against wild-type and mutant melanoma cell lines B16-F10, MeWo, SK-MEL-2, A2058c, and A375c are 2.7, 6.0, 3.9, 3.1, and 2.5 μM, respectively. DETD-35 holds promise for research in the field of anti-melanoma therapy .

HY-176724

ZnPc-O3-JQ1	Epigenetic Reader Domain Reactive Oxygen Species (ROS) HIF/HIF Prolyl-Hydroxylase	Cancer
ZnPc-O3-JQ1 is a light-triggered BRD4 degrader. Under illumination, ZnPc-O3-JQ1 generates reactive oxygen species (ROS) that degrades BRD4. The degradation of BRD4 results in downregulation of HIF-1α, thereby counteracting the photodynamic therapy (PDT) resistance induced by tumor hypoxia. ZnPc-O3-JQ1 exhibits both Type I and Type II PDT mechanisms. The structure of ZnPc-O3-JQ1 consists of three parts: BRD4 ligand (HY-78695); Linker (HY-W040165); Photosensitizer (HY-176725) .

HY-116497

PH11	FAK	Cancer
PH11 is a novel focal adhesion kinase (FAK) inhibitor that rapidly induces apoptosis in TRAIL-resistant PANC-1 cells when combined with TRAIL, but has no effect on normal human fibroblasts. The study found that PH11 downregulates c-FLIP through inhibition of FAK and phosphatidylinositol-3-kinase (PI3K)/AKT pathways, thereby restoring the TRAIL apoptotic pathway, suggesting that this combination therapy may provide an attractive therapeutic strategy for the safe and effective treatment of pancreatic cancer. PH11 selectively inhibits c-FLIP expression by modulating upstream signaling pathways and may represent an innovative therapeutic strategy. Although further work is needed to fully elucidate the mechanism of PH11-induced TRAIL sensitization, we believe that our results will provide a new approach to target c-FLIP without the risk of interfering with caspase-8 processing, which could potentially lead to TRAIL resistance. This study also suggests a role for the FAK/AKT signaling pathway in regulating c-FLIP expression in TRAIL-induced apoptosis, and this understanding will provide important clues to control the resistance mechanism to optimize the potential of TRAIL-based pancreatic cancer treatment.

HY-176785S

MCB-294	Ras Apoptosis p38 MAPK Caspase TNF Receptor	Cancer
MCB-294 is a dual-state pan-KRAS inhibitor that selectively inhibits KRAS over NRAS and HRAS. MCB-294 capable of binding both the active (GTP-bound) and inactive (GDP-bound) forms of KRAS with K_ds of approximately 1 pM and 10 nM, respectively. MCB-294 broadly impairs the growth of hTERT-HPNE cells expressing G12D, G12C, G12V, G12S, G13D, and wild-type KRAS, with IC₅₀s of approximately 700 nM. MCB-294 induces irreversible apoptosis in KRAS-mutated tumors. MCB-294 effectively suppress KRAS ^G12C inhibitor-resistant cancer cells and remodel the tumor immune microenvironment. MCB-294 can be used for the study of pancreatic cancer, colorectal cancer and lung cancer .

HY-176786

MCB-36	PROTACs Ras Apoptosis PERK p38 MAPK Caspase TNF Receptor	Cancer
MCB-36 is a VHL-recruiting pan-KRAS PROTAC degrader without affecting KRAS transcription. MCB-36 exhibits minimal effects on HRAS and NRAS protein levels. MCB-36 binds to the GDP-loaded state of G12D, G12C, G12V, and wild-type KRAS with high affinities K_d ≈ 1 pM). MCB-36 decreases p-ERK levels, leading to cell apoptosis. MCB-36 effectively suppress KRAS ^G12C inhibitor-resistant cancer cells and remodel the tumor immune microenvironment. MCB-36 can be used for the study of colorectal cancer and lung cancer (Pink: Target protein ligand; Blue: E3 ligand (HY-112078); Black: Linker (HY-W091879)) .

Cat. No.	Product Name

HY-L048

Antifungal Compound Library	450 compounds
The high rates of morbidity and mortality caused by fungal infections are associated with the current limited antifungal arsenal and the high toxicity of the compounds. Additionally, identifying novel drug targets is challenging because there are many similarities between fungal and human cells. The most common antifungal targets include fungal RNA synthesis and cell wall and membrane components, though new antifungal targets are being investigated. Nonetheless, fungi have developed resistance mechanisms, such as overexpression of efflux pump proteins, overexpression and changes in drug targets and biofilm formation, emphasizing the importance of discovering new antifungal drugs and therapies. Due to the limited antifungal arsenal, researchers have sought to improve treatment via different approaches, such as the combination of antifungal drugs, development of new formulations for antifungal agents and modifications to the chemical structures of traditional antifungals, etc. MCE offers a unique collection of 450 compounds with validated antifungal activities. MCE antifungal compound library is an effective tool for drug repurposing screening, combination screening and biological investigation.

Antifungal Compound Library

450 compounds

The high rates of morbidity and mortality caused by fungal infections are associated with the current limited antifungal arsenal and the high toxicity of the compounds. Additionally, identifying novel drug targets is challenging because there are many similarities between fungal and human cells. The most common antifungal targets include fungal RNA synthesis and cell wall and membrane components, though new antifungal targets are being investigated. Nonetheless, fungi have developed resistance mechanisms, such as overexpression of efflux pump proteins, overexpression and changes in drug targets and biofilm formation, emphasizing the importance of discovering new antifungal drugs and therapies. Due to the limited antifungal arsenal, researchers have sought to improve treatment via different approaches, such as the combination of antifungal drugs, development of new formulations for antifungal agents and modifications to the chemical structures of traditional antifungals, etc.

MCE offers a unique collection of 450 compounds with validated antifungal activities. MCE antifungal compound library is an effective tool for drug repurposing screening, combination screening and biological investigation.

Cat. No.	Product Name	Chemical Structure

HY-176785S

MCB-294
MCB-294 is a dual-state pan-KRAS inhibitor that selectively inhibits KRAS over NRAS and HRAS. MCB-294 capable of binding both the active (GTP-bound) and inactive (GDP-bound) forms of KRAS with K_ds of approximately 1 pM and 10 nM, respectively. MCB-294 broadly impairs the growth of hTERT-HPNE cells expressing G12D, G12C, G12V, G12S, G13D, and wild-type KRAS, with IC₅₀s of approximately 700 nM. MCB-294 induces irreversible apoptosis in KRAS-mutated tumors. MCB-294 effectively suppress KRAS ^G12C inhibitor-resistant cancer cells and remodel the tumor immune microenvironment. MCB-294 can be used for the study of pancreatic cancer, colorectal cancer and lung cancer .

MCB-294

MCB-294 is a dual-state pan-KRAS inhibitor that selectively inhibits KRAS over NRAS and HRAS. MCB-294 capable of binding both the active (GTP-bound) and inactive (GDP-bound) forms of KRAS with K_ds of approximately 1 pM and 10 nM, respectively. MCB-294 broadly impairs the growth of hTERT-HPNE cells expressing G12D, G12C, G12V, G12S, G13D, and wild-type KRAS, with IC₅₀s of approximately 700 nM. MCB-294 induces irreversible apoptosis in KRAS-mutated tumors. MCB-294 effectively suppress KRAS ^G12C inhibitor-resistant cancer cells and remodel the tumor immune microenvironment. MCB-294 can be used for the study of pancreatic cancer, colorectal cancer and lung cancer .

Cat. No.	Product Name		Classification

HY-176785S

MCB-294		Alkynes
MCB-294 is a dual-state pan-KRAS inhibitor that selectively inhibits KRAS over NRAS and HRAS. MCB-294 capable of binding both the active (GTP-bound) and inactive (GDP-bound) forms of KRAS with K_ds of approximately 1 pM and 10 nM, respectively. MCB-294 broadly impairs the growth of hTERT-HPNE cells expressing G12D, G12C, G12V, G12S, G13D, and wild-type KRAS, with IC₅₀s of approximately 700 nM. MCB-294 induces irreversible apoptosis in KRAS-mutated tumors. MCB-294 effectively suppress KRAS ^G12C inhibitor-resistant cancer cells and remodel the tumor immune microenvironment. MCB-294 can be used for the study of pancreatic cancer, colorectal cancer and lung cancer .

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