Cancer therapy resistance

By Targets:	Akt (1) Apoptosis (4) Caspase (2) ERK (1) Estrogen Receptor/ERR (1) FAK (1) Ferroptosis (1) FGFR (1) Glutathione Peroxidase (1) Microtubule/Tubulin (1) p38 MAPK (2) PERK (1) PI3K (1) PROTACs (1) Ras (2) Reactive Oxygen Species (ROS) (1) STAT (1) TNF Receptor (2)
By Research Areas:	Cancer (9)
Click Chemistry:	Alkynes (3)

Targets Recommended: BCRP P-glycoprotein

Cat. No.	Product Name	Target	Research Areas	Chemical Structure

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)) .

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-175633

ML210-ansaFc	Glutathione Peroxidase Ferroptosis Reactive Oxygen Species (ROS)	Cancer
ML210-ansaFc (Compound III-13) is a covalent GPX4 inhibitor with a -ferrocenophane group (IC₅₀ of 3.4 μM). ML210-ansaFc potently induces ferroptosis by increasing the level of ROSand promoting lipid peroxidation (LPO) in cancers cells. ML210-ansaFc has an anticancer activity and suppresses tumor growth in tumor 3D spheroids. ML210-ansaFc can be used for cancer therapy resistance research .

HY-176955

ER degrader 12	Estrogen Receptor/ERR	Cancer
ER degrader 12 (Example 1) is an estrogen receptor (ER) degrader with IC₅₀ values for ERα and ERβ of 2.3 and 80.2 nM respectively (TR-FRET experiment). ER degrader 12 inhibits the proliferation of MCF-7 cells, with an IC₅₀ of 1.53 nM. ER degrader 12 can be used for research on breast cancer .

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-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-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-15244G

Alpelisib	PI3K Apoptosis	Cancer
Alpelisib GMP is Alpelisib (HY-15244) produced by using GMP guidelines. GMP small molecules works appropriately as an auxiliary reagent for cell therapy manufacture. Alpelisib (BYL-719) is an orally active PI3Kα-selective inhibitor that blocks the conversion of PIP2 to PIP3, thereby inhibiting pathways including PI3K/AKT/mTOR, MAPK/ERK, Notch and JAK-STAT. Alpelisib also induces apoptosis, G0/G1 phase arrest and senescence; it significantly inhibits the proliferation, self-renewal, stemness and epithelial-mesenchymal transition (EMT) of tumor cells, reduces cancer stem cell populations and decreases the expression of stem cell markers. Alpelisib not only enhances the sensitivity to Eribulin (HY-13442) and exerts a synergistic effect with Paclitaxel (HY-B0015), but may also induce drug resistance by upregulating the SGK3/GSK3β/β-catenin signaling pathway. Alpelisib can be applied to research related to breast cancer, gastric cancer and lipomas associated with PTEN hamartoma tumor syndrome .

Cat. No.	Product Name	Type

HY-15244G

Alpelisib	Fluorescent Dyes
Alpelisib GMP is Alpelisib (HY-15244) produced by using GMP guidelines. GMP small molecules works appropriately as an auxiliary reagent for cell therapy manufacture. Alpelisib (BYL-719) is an orally active PI3Kα-selective inhibitor that blocks the conversion of PIP2 to PIP3, thereby inhibiting pathways including PI3K/AKT/mTOR, MAPK/ERK, Notch and JAK-STAT. Alpelisib also induces apoptosis, G0/G1 phase arrest and senescence; it significantly inhibits the proliferation, self-renewal, stemness and epithelial-mesenchymal transition (EMT) of tumor cells, reduces cancer stem cell populations and decreases the expression of stem cell markers. Alpelisib not only enhances the sensitivity to Eribulin (HY-13442) and exerts a synergistic effect with Paclitaxel (HY-B0015), but may also induce drug resistance by upregulating the SGK3/GSK3β/β-catenin signaling pathway. Alpelisib can be applied to research related to breast cancer, gastric cancer and lipomas associated with PTEN hamartoma tumor syndrome .

Alpelisib

Fluorescent Dyes

Alpelisib GMP is Alpelisib (HY-15244) produced by using GMP guidelines. GMP small molecules works appropriately as an auxiliary reagent for cell therapy manufacture. Alpelisib (BYL-719) is an orally active PI3Kα-selective inhibitor that blocks the conversion of PIP2 to PIP3, thereby inhibiting pathways including PI3K/AKT/mTOR, MAPK/ERK, Notch and JAK-STAT. Alpelisib also induces apoptosis, G0/G1 phase arrest and senescence; it significantly inhibits the proliferation, self-renewal, stemness and epithelial-mesenchymal transition (EMT) of tumor cells, reduces cancer stem cell populations and decreases the expression of stem cell markers. Alpelisib not only enhances the sensitivity to Eribulin (HY-13442) and exerts a synergistic effect with Paclitaxel (HY-B0015), but may also induce drug resistance by upregulating the SGK3/GSK3β/β-catenin signaling pathway. Alpelisib can be applied to research related to breast cancer, gastric cancer and lipomas associated with PTEN hamartoma tumor syndrome .

Cat. No.	Product Name	Type

HY-15244G

Alpelisib	Biochemical Assay Reagents
Alpelisib GMP is Alpelisib (HY-15244) produced by using GMP guidelines. GMP small molecules works appropriately as an auxiliary reagent for cell therapy manufacture. Alpelisib (BYL-719) is an orally active PI3Kα-selective inhibitor that blocks the conversion of PIP2 to PIP3, thereby inhibiting pathways including PI3K/AKT/mTOR, MAPK/ERK, Notch and JAK-STAT. Alpelisib also induces apoptosis, G0/G1 phase arrest and senescence; it significantly inhibits the proliferation, self-renewal, stemness and epithelial-mesenchymal transition (EMT) of tumor cells, reduces cancer stem cell populations and decreases the expression of stem cell markers. Alpelisib not only enhances the sensitivity to Eribulin (HY-13442) and exerts a synergistic effect with Paclitaxel (HY-B0015), but may also induce drug resistance by upregulating the SGK3/GSK3β/β-catenin signaling pathway. Alpelisib can be applied to research related to breast cancer, gastric cancer and lipomas associated with PTEN hamartoma tumor syndrome .

Alpelisib

Biochemical Assay Reagents

Alpelisib GMP is Alpelisib (HY-15244) produced by using GMP guidelines. GMP small molecules works appropriately as an auxiliary reagent for cell therapy manufacture. Alpelisib (BYL-719) is an orally active PI3Kα-selective inhibitor that blocks the conversion of PIP2 to PIP3, thereby inhibiting pathways including PI3K/AKT/mTOR, MAPK/ERK, Notch and JAK-STAT. Alpelisib also induces apoptosis, G0/G1 phase arrest and senescence; it significantly inhibits the proliferation, self-renewal, stemness and epithelial-mesenchymal transition (EMT) of tumor cells, reduces cancer stem cell populations and decreases the expression of stem cell markers. Alpelisib not only enhances the sensitivity to Eribulin (HY-13442) and exerts a synergistic effect with Paclitaxel (HY-B0015), but may also induce drug resistance by upregulating the SGK3/GSK3β/β-catenin signaling pathway. Alpelisib can be applied to research related to breast cancer, gastric cancer and lipomas associated with PTEN hamartoma tumor syndrome .

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-176786

MCB-36		Alkynes
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)) .

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 .

HY-175633

ML210-ansaFc		Alkynes
ML210-ansaFc (Compound III-13) is a covalent GPX4 inhibitor with a -ferrocenophane group (IC₅₀ of 3.4 μM). ML210-ansaFc potently induces ferroptosis by increasing the level of ROSand promoting lipid peroxidation (LPO) in cancers cells. ML210-ansaFc has an anticancer activity and suppresses tumor growth in tumor 3D spheroids. ML210-ansaFc can be used for cancer therapy resistance research .

Targets Recommended: BCRP P-glycoprotein

Cat. No.	Product Name	Target	Research Areas	Chemical Structure

HY-15244G

Alpelisib	PI3K Apoptosis	Cancer
Alpelisib GMP is Alpelisib (HY-15244) produced by using GMP guidelines. GMP small molecules works appropriately as an auxiliary reagent for cell therapy manufacture. Alpelisib (BYL-719) is an orally active PI3Kα-selective inhibitor that blocks the conversion of PIP2 to PIP3, thereby inhibiting pathways including PI3K/AKT/mTOR, MAPK/ERK, Notch and JAK-STAT. Alpelisib also induces apoptosis, G0/G1 phase arrest and senescence; it significantly inhibits the proliferation, self-renewal, stemness and epithelial-mesenchymal transition (EMT) of tumor cells, reduces cancer stem cell populations and decreases the expression of stem cell markers. Alpelisib not only enhances the sensitivity to Eribulin (HY-13442) and exerts a synergistic effect with Paclitaxel (HY-B0015), but may also induce drug resistance by upregulating the SGK3/GSK3β/β-catenin signaling pathway. Alpelisib can be applied to research related to breast cancer, gastric cancer and lipomas associated with PTEN hamartoma tumor syndrome .

MCE Japan Authorized Agent ナミキ商事株式会社コスモ・バイオ株式会社重松貿易株式会社
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Fluorescent Dyes

Biochemical Assay Reagents

Isotope-Labeled Compounds

Click Chemistry

GMP Molecules

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