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gastric cancer model

" in MedChemExpress (MCE) Product Catalog:

26

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2

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8

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1

Isotope-Labeled Compounds

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Cat. No. Product Name Target Research Areas Chemical Structure
  • HY-P1727
    Super-TDU
    4 Publications Verification

    		 YAP Cancer
    Super-TDU is a specific YAP antagonist targeting YAP-TEADs interaction. Super-TDU suppresses tumor growth in gastric cancer mouse model .
    Super-TDU
  • HY-153190
    W1131

    		Oxidative Phosphorylation STAT Ferroptosis Cancer
    W1131 is a potent STAT3 inhibitor, triggering ferroptosis. W1131 suppresses cancer progression in gastric cancer cell subcutaneous xenograft model, organoids model, and PDX model. W1131 effectively alleviates chemical resistance of cancer cells to 5-FU (HY-90006). W1131 regulates cell cycle, DNA damage response, and oxidative phosphorylation, including IL6-JAK-STAT3 pathway and ferroptosis pathway .
    W1131
  • HY-W013973
    p-Terphenyl

    		Fungal Cancer
    p-Terphenyl is a p-terphenyl that can be isolated from Aspergillus of the genus Thelephora. p-Terphenyl showed significant anti-tumor and anti-metastatic effects in xenograft models of gastric and pancreatic cancer. Derivatives of p-Terphenyl also have anti-inflammatory or anti-proliferative effects .
    p-Terphenyl
  • HY-164285
    MYX1715

    		ADC Cytotoxin N-myristoyltransferase Cancer
    MYX1715 is an inhibitor of N-Myristoyltransferase (NMT) with a KD value of 0.09 nM. MYX1715 inhibits the proliferation of LU0884 and LU2511 with IC50 values of 44 nM and 9 nM. MYX1715 exhibits antitumor efficacy against neuroblastoma and gastric cancer in mouse models. MYX1715 can be used as ADC toxin .
    MYX1715
  • HY-153190A
    W1131 TFA

    		Ferroptosis STAT Cancer
    W1131 TFA is a potent STAT3 inhibitor that induces ferroptosis. W1131 inhibits cancer progression in subcutaneous xenograft, organoid, and PDX models of gastric cancer. W1131 effectively alleviates cancer cell chemoresistance to 5-FU (HY-90006). W1131 regulates the cell cycle, DNA damage response, and oxidative phosphorylation, including the IL6-JAK-STAT3 pathway and the ferroptosis pathway .
    W1131 TFA
  • HY-172916
    LC-SF-14

    		SHP2 FGFR p38 MAPK ERK Cancer
    LC-SF-14 is a selective dual inhibitor of SHP2 and FGFR (IC50 values are 71.6 and 8.9 nM, respectively). LC-SF-14 inhibits FGFR2-FRS2α-SHP2-MAPK signaling and ERK phosphorylation. LC-SF-14 inhibits the proliferation of KATOIII cancer cells (IC50: 9.2 nM). LC-SF-14 has antitumor activity in the SNU-16 xenograft mouse model. LC-SF-14 can be used in FGFR2-driven gastric cancer research .
    LC-SF-14
  • HY-P1727A
    Super-TDU TFA

    		YAP Cancer
    Super-TDU TFA is a specific YAP antagonist targeting YAP-TEADs interaction. Super-TDU TFA suppresses tumor growth in gastric cancer mouse model .
    Super-TDU TFA
  • HY-P1728
    Super-TDU (1-31)

    		YAP Cancer
    Super-TDU (1-31) is a peptide fragment of Super-TDU. Super-TDU (1-31) is an inhibitor of YAP-TEAD complex. Super-TDU shows potent anti-tumor activity and suppresses tumor growth in gastric cancer mouse model .
    Super-TDU (1-31)
  • HY-119618
    R1498

    		Endogenous Metabolite Cancer
    R1498 is a multi-target kinase inhibitor with anti-angiogenic and anti-proliferative activities. R1498 mainly targets targets such as Aurora kinase and VEGFR2, which are associated with tumor development. R1498 showed moderate in vitro growth inhibition in a variety of tumor cells, with IC50 values in the micromolar range. R1498 showed anti-tumor efficacy superior to sorafenib in a variety of gastric cancer and hepatocellular carcinoma xenograft models, with tumor growth inhibition rates exceeding 80%, and tumor shrinkage was observed in some models. R1498 showed a 10-30% tumor shrinkage rate in three xenograft models derived from human primary gastric cancer tumors, further demonstrating its inhibitory potential. R1498 effectively inhibited Aurora A activity in vivo and reduced tumor vascularization .
    R1498
  • HY-P1728A
    Super-TDU (1-31) TFA

    		YAP Cancer
    Super-TDU (1-31) TFA is a peptide fragment of Super-TDU. Super-TDU (1-31) TFA is an inhibitor of YAP-TEAD complex. Super-TDU TFA shows potent anti-tumor activity and suppresses tumor growth in gastric cancer mouse model .
    Super-TDU (1-31) TFA
  • HY-164411
    KRC-00715

    		c-Met/HGFR Cancer
    KRC-00715 is an effective oral c-Met inhibitor with an IC50 of 9.0 nM, demonstrating high selectivity in gastric cancer cells. KRC-00715 specifically inhibits the growth of c-Met-highly expressed cell lines by inducing G1/S phase arrest, leading to a reduction in downstream signaling pathways, including Akt and Erk, as well as c-Met activity. KRC-00715, in the gastric cancer cell line Hs746, is characterized by an IC50 of 39 nM, and it selectively inhibits the proliferation of c-Met-highly expressed cell lines. KRC-00715 reduces tumor size in Hs746T xenograft mouse models .
    KRC-00715
  • HY-W013973R
    p-Terphenyl (Standard)

    		Fungal Reference Standards Cancer
    p-Terphenyl (Standard) is the analytical standard of p-Terphenyl. This product is intended for research and analytical applications. p-Terphenyl is a p-terphenyl that can be isolated from Aspergillus of the genus Thelephora. p-Terphenyl showed significant anti-tumor and anti-metastatic effects in xenograft models of gastric and pancreatic cancer. Derivatives of p-Terphenyl also have anti-inflammatory or anti-proliferative effects .
    p-Terphenyl (Standard)
  • HY-147040
    ABN401

    		c-Met/HGFR Apoptosis Cancer
    ABN401 is an orally active and selective ATP-competitive c-MET inhibitor with an IC50 of 10 nM. ABN401 is cytotoxic to MET-addicted cancer cells with the IC50 of 2-43 nM. ABN401 has bioavailability in rats and dogs of 42.1-56.2% and 27.4-37.7%, respectively. ABN401 has antitumor activity .
    ABN401
  • HY-100555
    CH5138303

    		HSP Infection Cancer
    CH5138303 is a potent and orally active Hsp90 inhibitor. CH5138303 shows high binding affinity for N-terminal Hsp90α, with Kd of 0.52 nM. CH5138303 shows potent anti-proliferative activity against human cancer cell lines (HCT116 and NCI-N87), with IC50 values of 0.098 and 0.066 μM, respectively. CH5138303 shows high oral bioavailability in mice (F=44.0%). CH5138303 shows potent antitumor efficacy in a human NCI-N87 gastric cancer xenograft model .
    CH5138303
  • HY-N4247
    Kuwanon G

    		Bombesin Receptor Bacterial Apoptosis Reactive Oxygen Species (ROS) PI3K Akt GSK-3 MMP mTOR NF-κB LXR Infection Cardiovascular Disease Neurological Disease Inflammation/Immunology Cancer
    Kuwanon G is a flavonoid compound and an antagonist of the bombesin receptor. Kuwanon G has multiple activities such as bactericidal, anti-tumor, anti-inflammatory, antioxidant, anti-atherosclerotic, and neuroprotective effects. Kuwanon G exhibits strong antibacterial activity against oral pathogens, especially cariogenic bacteria and periodontal pathogens. Kuwanon G can induce apoptosis and inhibit proliferation, migration, and invasion of tumor cells. Kuwanon G can be used in the research of diseases such as gastric cancer and atherosclerosis .
    Kuwanon G
  • HY-170954
    C-Met/Axl-IN-1

    		Apoptosis c-Met/HGFR TAM Receptor Cancer
    C-Met/Axl-IN-1 (Compound 22a) is an orally active and selective type II c-Met/Axl inhibitor with IC50 values of 1 nM and 10 nM, respectively. C-Met/Axl-IN-1 can inhibit proliferation, induce cell cycle arrest and apoptosis of tumor cells. C-Met/Axl-IN-1 has strong anti-tumor activity .
    C-Met/Axl-IN-1
  • HY-170919
    FGFR2/3-IN-2

    		FGFR Cancer
    FGFR2/3-IN-2 (compound 10) is an orally active FGFR2 and FGFR3 inhibitor. FGFR2/3-IN-2 inhibits FGFR2 and FGFR3 with IC50s of 3.7 nM and 31.2 nM (preincubation time 1 h), respectively. FGFR2/3-IN-2 spares FGFR1/4 and other kinases without causing diarrhea and serum phosphate elevation in vivo. FGFR2/3-IN-2 induces tumor stasis or regression in the SNU-16 gastric cancer model .
    FGFR2/3-IN-2
  • HY-176237
    Nampt-IN-16

    		NAMPT Apoptosis Cancer
    Nampt-IN-16 (Compound 9a) is an orally active NAMPT inhibitor with an IC50 of 0.15 μM. Nampt-IN-16 can reduce intracellular NAD + and ATP levels. Nampt-IN-16 can inhibit the proliferation, migration, and invasion, induce cell cycle arrest and apoptosis, and alter cellular metabolism of gastric cancer cells. Nampt-IN-16 can be used in the research of tumors such as gastric cancer .
    Nampt-IN-16
  • HY-160506
    PRO-6E

    		PROTACs c-Met/HGFR Apoptosis Cancer
    PRO-6E is an oral active PROTAC based on Cereblon ligand, and induces the degradation of MET with maximum degradation of 81.9% at 1 μM in MKN-45 cells. PRO-6E inhibits tumor growth in vivo and in vitro. PRO-6E induces cell apoptosis and induces cell arrest (Sturcture Note:(Blue: Cereblon ligand (HY-103596), Black: linker；Pink: ALK/c-Met inhibitor Crizotinib (HY-50878)) .
    PRO-6E
  • HY-144099
    Keap1-Nrf2-IN-4

    		E1/E2/E3 Enzyme Apoptosis Cancer
    Keap1-Nrf2-IN-4 is a potent neddylation inhibitor. Keap1-Nrf2-IN-4 exhibits potent anti-proliferation activity against MGC-803 cells (IC50=2.55 µM). Keap1-Nrf2-IN-4 blocks the migration ability and induces apoptosis of gastric cancer cells. Keap1-Nrf2-IN-4 inhibits tumor growth without obvious toxicity .
    Keap1-Nrf2-IN-4
  • HY-114118B
    Semaglutide acetate
    Maximum Cited Publications
    14 Publications Verification

    		 GLP Receptor Insulin Receptor α-synuclein Apoptosis p38 MAPK Autophagy Bcl-2 Family Neurological Disease Metabolic Disease Cancer
    Semaglutide acetate is a long-acting, selective, competitive, orally active GLP-1R agonist that can penetrate the blood-brain barrier. After activating GLP-1R, Semaglutide acetate promotes insulin secretion, inhibits gastric emptying and appetite, and at the same time enhances autophagy, inhibits oxidative stress and apoptosis. Semaglutide acetate also regulates mitochondrial function and lipid metabolism (such as reducing de novo lipogenesis in the liver). Semaglutide acetate has activities such as lowering blood sugar, reducing weight, neuroprotection (such as improving motor function in Parkinson's disease models, reducing α-synuclein aggregation) and improving hepatic steatosis. Semaglutide acetate can be used for the study of neurodegenerative diseases and liver diseases such as type 2 diabetes, obesity, Parkinson's disease, metabolic associated fatty liver disease (MASLD), and cancer .
    Semaglutide acetate
  • HY-114118
    Semaglutide
    Maximum Cited Publications
    14 Publications Verification

    		 GLP Receptor Insulin Receptor α-synuclein Apoptosis p38 MAPK Autophagy Bcl-2 Family Neurological Disease Metabolic Disease Cancer
    Semaglutide is a long-acting, selective, competitive, orally active GLP-1R agonist that can penetrate the blood-brain barrier. After activating GLP-1R, Semaglutide promotes insulin secretion, inhibits gastric emptying and appetite, and at the same time enhances autophagy, inhibits oxidative stress and apoptosis. Semaglutide also regulates mitochondrial function and lipid metabolism (such as reducing de novo lipogenesis in the liver). Semaglutide has activities such as lowering blood sugar, reducing weight, neuroprotection (such as improving motor function in Parkinson's disease models, reducing α-synuclein aggregation) and improving hepatic steatosis. Semaglutide can be used for the study of neurodegenerative diseases and liver diseases such as type 2 diabetes, obesity, Parkinson's disease, metabolic associated fatty liver disease (MASLD), and cancer .
    Semaglutide
  • HY-114118A
    Semaglutide TFA
    Maximum Cited Publications
    14 Publications Verification

    		 GLP Receptor Insulin Receptor α-synuclein Apoptosis p38 MAPK Autophagy Bcl-2 Family Neurological Disease Metabolic Disease Cancer
    Semaglutide TFA is a long-acting, selective, competitive, orally active GLP-1R agonist that can penetrate the blood-brain barrier. After activating GLP-1R, Semaglutide TFA promotes insulin secretion, inhibits gastric emptying and appetite, and at the same time enhances autophagy, inhibits oxidative stress and apoptosis. Semaglutide TFA also regulates mitochondrial function and lipid metabolism (such as reducing de novo lipogenesis in the liver). Semaglutide TFA has activities such as lowering blood sugar, reducing weight, neuroprotection (such as improving motor function in Parkinson's disease models, reducing α-synuclein aggregation) and improving hepatic steatosis. Semaglutide TFA can be used for the study of neurodegenerative diseases and liver diseases such as type 2 diabetes, obesity, Parkinson's disease, metabolic associated fatty liver disease (MASLD), and cancer .
    Semaglutide TFA
  • HY-114118F
    Semaglutide, FITC labeled

    		GLP Receptor Insulin Receptor α-synuclein Apoptosis p38 MAPK Autophagy Bcl-2 Family Neurological Disease Metabolic Disease Cancer
    Semaglutide, FITC labeled is a long-acting, selective, competitive, orally active GLP-1R agonist that can penetrate the blood-brain barrier. After activating GLP-1R, Semaglutide, FITC labeled promotes insulin secretion, inhibits gastric emptying and appetite, and at the same time enhances autophagy, inhibits oxidative stress and apoptosis. Semaglutide, FITC labeled also regulates mitochondrial function and lipid metabolism (such as reducing de novo lipogenesis in the liver). Semaglutide, FITC labeled has activities such as lowering blood sugar, reducing weight, neuroprotection (such as improving motor function in Parkinson's disease models, reducing α-synuclein aggregation) and improving hepatic steatosis. Semaglutide, FITC labeled can be used for the study of neurodegenerative diseases and liver diseases such as type 2 diabetes, obesity, Parkinson's disease, metabolic associated fatty liver disease (MASLD), and cancer .
    Semaglutide, FITC labeled
  • HY-163985
    PROTAC FGFR2 degrader 1

    		PROTACs FGFR Apoptosis Cancer
    PROTAC FGFR2 degrader 1 (compound N5) is a PROTAC that effectively targets FGFR2 with DC50 of 6.46 nM, the FGFR2 IC50 is 0.08 nM. PROTAC FGFR2 degrader 1 has anti-proliferative activity and highly selective, induces G0/G1 arrest of KATOIII and SNU16 cell cycle and inhibits apoptosis by reducing the activation of p-ERK and p-PLCγ, the downstream proteins of FGFR2. PROTAC FGFR2 degrader 1 inhibits gastric cancer cells remained above 50% at a concentration of 0.17 nM. PROTAC FGFR2 degrader 1 potently inhibits the growth of SNU16 xenograft tumors in mouse model (Structure Note: Pink, FGFR2 activator: HY-18708; Blue, E3 ligase ligand: HY--10984; Black, linker: HY-163989; E3 ligase ligand + linker：HY-163986) .
    PROTAC FGFR2 degrader 1
  • HY-114118S3
    Semaglutide-13C6,15N TFA

    		Isotope-Labeled Compounds GLP Receptor Insulin Receptor α-synuclein Apoptosis p38 MAPK Autophagy Bcl-2 Family Metabolic Disease
    Semaglutide- 13C6, 15N TFA is the 13C- and 15N-labeled Semaglutide TFA (HY-114118A). Semaglutide TFA is a long-acting, selective, competitive, orally active GLP-1R agonist that can penetrate the blood-brain barrier. After activating GLP-1R, Semaglutide TFA promotes insulin secretion, inhibits gastric emptying and appetite, and at the same time enhances autophagy, inhibits oxidative stress and apoptosis. Semaglutide TFA also regulates mitochondrial function and lipid metabolism (such as reducing de novo lipogenesis in the liver). Semaglutide TFA has activities such as lowering blood sugar, reducing weight, neuroprotection (such as improving motor function in Parkinson's disease models, reducing α-synuclein aggregation) and improving hepatic steatosis. Semaglutide TFA can be used for the study of neurodegenerative diseases and liver diseases such as type 2 diabetes, obesity, Parkinson's disease, metabolic associated fatty liver disease (MASLD), and cancer .
    Semaglutide-13C6,15N TFA

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