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caspase-3/p53

" in MedChemExpress (MCE) Product Catalog:

71

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1

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2

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5

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Cat. No. Product Name Target Research Areas Chemical Structure
  • HY-N1423
    Glycocholic acid
    3 Publications Verification

    		 P-glycoprotein Bcl-2 Family G protein-coupled Bile Acid Receptor 1 Endogenous Metabolite Bacterial Apoptosis FXR Caspase MDM-2/p53 LPL Receptor Metabolic Disease Inflammation/Immunology Cancer
    Glycocholic acid is a bile acid derivative. Glycocholic acid downregulates MDR1, Bcl-2, MRP1, MRP2 and FXR, upregulates Bax, p53, caspase-9, caspase-3, TGR5 and S1PR2. Glycocholic acid inhibits multidrug resistance and efflux pumps, induces mitochondrial apoptosis, and enhances chemosensitivity. Glycocholic acid modulates related bile acid receptor signaling. Glycocholic acid suppresses growth and conjugation of Enterobacteriaceae and increases their antibiotic susceptibility. Glycocholic acid can be used for the research of colon adenocarcinoma and cholangiocarcinoma (CCA) [3].
    Glycocholic acid
  • HY-N0171A
    Beta-Sitosterol (purity>98%)
    15+ Cited Publications

    β-Sitosterol (purity>98%); 22,23-Dihydrostigmasterol (purity>98%)

    		 Bacterial Apoptosis Reactive Oxygen Species (ROS) MDM-2/p53 Caspase PARP MMP Bcl-2 Family HIF/HIF Prolyl-Hydroxylase TNF Receptor Interleukin Related NF-κB mTOR Lactate Dehydrogenase CDK Glutathione Peroxidase SOD Infection Cardiovascular Disease Inflammation/Immunology Cancer
    Beta-Sitosterol (purity>98%) is orally active. Beta-Sitosterol exhibits multiple activities, including anti-inflammatory, anticancer, antioxidant, antimicrobial, antidiabetic, antioxidant enzyme, and analgesic. Beta-Sitosterol inhibits inflammation and impaired adipogenesis in bovine mammary epithelial cells by reducing levels of ROS, TNF-α, IL-1β, and NF-κB p65 and restoring the activity of the HIF-1α/mTOR signaling pathway. Beta-Sitosterol induces apoptosis in cancer cells through ROS-mediated mitochondrial dysregulation and p53 activation. Beta-Sitosterol exerts its anticancer effects in cancer cells by activating caspase-3, caspase-8, and caspase-9, mediating PARP inactivation, MMP loss, altered Bcl-2-Bax ratio, and cytochrome c release. Beta-Sitosterol modulates macrophage polarization and reduces rheumatoid inflammation in mice. Beta-Sitosterol inhibits tumor growth in multiple mouse cancer models. Beta-Sitosterol can be used in the research of arthritis, lung cancer, breast cancer and other cancers, diabetes, etc [3] .
    Beta-Sitosterol (purity>98%)
  • HY-N0171
    Beta-Sitosterol (purity>80%)
    20+ Cited Publications

    		 Apoptosis Endogenous Metabolite Cardiovascular Disease Inflammation/Immunology Cancer
    Beta-Sitosterol (purity≥80%) is orally active. Beta-Sitosterol exhibits multiple activities, including anti-inflammatory, anticancer, antioxidant, antimicrobial, antidiabetic, antioxidant enzyme, and analgesic. Beta-Sitosterol inhibits inflammation and impaired adipogenesis in bovine mammary epithelial cells by reducing levels of ROS, TNF-α, IL-1β, and NF-κB p65 and restoring the activity of the HIF-1α/mTOR signaling pathway. Beta-Sitosterol induces apoptosis in cancer cells through ROS-mediated mitochondrial dysregulation and p53 activation. Beta-Sitosterol exerts its anticancer effects in cancer cells by activating caspase-3, caspase-8, and caspase-9, mediating PARP inactivation, MMP loss, altered Bcl-2-Bax ratio, and cytochrome c release. Beta-Sitosterol modulates macrophage polarization and reduces rheumatoid inflammation in mice. Beta-Sitosterol inhibits tumor growth in multiple mouse cancer models. Beta-Sitosterol can be used in the research of arthritis, lung cancer, breast cancer and other cancers, diabetes, etc [3] .
    Beta-Sitosterol (purity>80%)
  • HY-D0848
    N,N'-Methylenebisacrylamide

    Bisacrylamide; MBA; Methylenebisacrylamide; N,N-Methylenebisacrylamide

    		 Biochemical Assay Reagents MDM-2/p53 Caspase Cardiovascular Disease Endocrinology Cancer
    N,N'-Methylenebisacrylamide (Bisacrylamide) is an orally active acrylamide dimer and crosslinker. N,N'-Methylenebisacrylamide increases CYP2E1, P53, cleaved caspase-3. N,N'-Methylenebisacrylamide promotes hepatic cancer. N,N'-Methylenebisacrylamide changes sperm abnormality rate and sperm count. N,N'-Methylenebisacrylamide decreases the number of various cells in the blood as well as induces liver and testicular damage. N,N'-Methylenebisacrylamide is used to prepare polyacrylamide gel [3] .
    N,N'-Methylenebisacrylamide
  • HY-135954A
    PDK4-IN-1 hydrochloride
    3 Publications Verification

    		 PDHK Apoptosis Metabolic Disease Inflammation/Immunology Cancer
    PDK4-IN-1 hydrochloride is an anthraquinone derivative and a potent and orally active pyruvate dehydrogenase kinase 4 (PDK4) inhibitor with an IC50 value of 84 nM. PDK4-IN-1 hydrochloride potently represses cellular transformation and cellular proliferation and induces apoptosis. PDK4-IN-1 hydrochloride has antidiabetic, anticancer and anti-allergic activity .
    PDK4-IN-1 hydrochloride
  • HY-135954
    PDK4-IN-1
    3 Publications Verification

    		 PDHK Apoptosis Metabolic Disease Inflammation/Immunology Cancer
    PDK4-IN-1 is an anthraquinone derivative and a potent and orally active pyruvate dehydrogenase kinase 4 (PDK4) inhibitor with an IC50 value of 84 nM. PDK4-IN-1 potently represses cellular transformation and cellular proliferation and induces apoptosis. PDK4-IN-1 has antidiabetic, anticancer and anti-allergic activity .
    PDK4-IN-1
  • HY-N1423A
    Glycocholic acid sodium
    3 Publications Verification

    		 P-glycoprotein Bcl-2 Family G protein-coupled Bile Acid Receptor 1 Bacterial Apoptosis FXR Caspase MDM-2/p53 LPL Receptor Endogenous Metabolite Metabolic Disease Cancer
    Glycocholic acid sodium is a bile acid derivative. Glycocholic acid downregulates MDR1, Bcl-2, MRP1, MRP2 and FXR, upregulates Bax, p53, caspase-9, caspase-3, TGR5 and S1PR2. Glycocholic acid sodium inhibits multidrug resistance and efflux pumps, induces mitochondrial apoptosis, and enhances chemosensitivity. Glycocholic acid sodium modulates related bile acid receptor signaling. Glycocholic acid sodium suppresses growth and conjugation of Enterobacteriaceae and increases their antibiotic susceptibility. Glycocholic acid sodium can be used for the research of colon adenocarcinoma and cholangiocarcinoma (CCA) [3].
    Glycocholic acid sodium
  • HY-N1423S
    Glycocholic acid-d4

    		Isotope-Labeled Compounds P-glycoprotein Bcl-2 Family G protein-coupled Bile Acid Receptor 1 Endogenous Metabolite Bacterial Apoptosis FXR Caspase MDM-2/p53 LPL Receptor Metabolic Disease Cancer
    Glycocholic acid-d4 is the deuterium labeled Glycocholic acid (HY-N1423). Glycocholic acid is a bile acid derivative. Glycocholic acid downregulates MDR1, Bcl-2, MRP1, MRP2 and FXR, upregulates Bax, p53, caspase-9, caspase-3, TGR5 and S1PR2. Glycocholic acid inhibits multidrug resistance and efflux pumps, induces mitochondrial apoptosis, and enhances chemosensitivity. Glycocholic acid modulates related bile acid receptor signaling. Glycocholic acid suppresses growth and conjugation of Enterobacteriaceae and increases their antibiotic susceptibility. Glycocholic acid can be used for the research of colon adenocarcinoma and cholangiocarcinoma (CCA).
    Glycocholic acid-d4
  • HY-N0171R
    Beta-Sitosterol (Standard)
    5+ Cited Publications

    β-Sitosterol (Standard); 22,23-Dihydrostigmasterol (Standard))

    		 Reference Standards Apoptosis Endogenous Metabolite Cardiovascular Disease Inflammation/Immunology Cancer
    Beta-Sitosterol (Standard) is the analytical standard of Beta-Sitosterol. This product is intended for research and analytical applications. Beta-Sitosterol (purity≥80%) is orally active. Beta-Sitosterol exhibits multiple activities, including anti-inflammatory, anticancer, antioxidant, antimicrobial, antidiabetic, antioxidant enzyme, and analgesic. Beta-Sitosterol inhibits inflammation and impaired adipogenesis in bovine mammary epithelial cells by reducing levels of ROS, TNF-α, IL-1β, and NF-κB p65 and restoring the activity of the HIF-1α/mTOR signaling pathway. Beta-Sitosterol induces apoptosis in cancer cells through ROS-mediated mitochondrial dysregulation and p53 activation. Beta-Sitosterol exerts its anticancer effects in cancer cells by activating caspase-3, caspase-8, and caspase-9, mediating PARP inactivation, MMP loss, altered Bcl-2-Bax ratio, and cytochrome c release. Beta-Sitosterol modulates macrophage polarization and reduces rheumatoid inflammation in mice. Beta-Sitosterol inhibits tumor growth in multiple mouse cancer models. Beta-Sitosterol can be used in the research of arthritis, lung cancer, breast cancer and other cancers, diabetes, etc.
    Beta-Sitosterol (Standard)
  • HY-B0960
    Sulfabenzamide
    1 Publications Verification

    N-Sulfanilylbenzamide

    		 Bacterial Autophagy MDM-2/p53 Caspase PARP DNA-PK Akt Infection Cancer
    Sulfabenzamide (N-Sulfanilylbenzamide) is a sulfonamide antibacterial agent. Sulfabenzamide exhibit antibacterial activity against Staphylococcus aureus (ATCC 25923) and Escherichia coli (ATCC 8739). Sulfabenzamide can promote autophagic cell autophagy in breast cancer cells through p53/ DRAM pathway. Sulfabenzamide increases caspase-3 activity, deactivates PARP1 and DNA-PK, downregulates AKT1 and AKT2. Sulfabenzamide can be used for the researches of breast cancer and bacterial infections .
    Sulfabenzamide
  • HY-119979
    Cardanol monoene

    Cardanol C15:1

    		 Apoptosis Reactive Oxygen Species (ROS) Mitochondrial Metabolism MMP CDK Caspase Bcl-2 Family PARP MDM-2/p53 Cholinesterase (ChE) Infection Inflammation/Immunology Cancer
    Cardanol monoene (Cardanol C15:1) is a phenolic compound which can be found in cashew nut shell liquid. Cardanol monoene can inhibit cancer cells proliferation, migration, cause S phase arrest, induce apoptosis, ROS production and mitochondrial depolarization. Cardanol monoene downregulates MMP-2, MMP-9, cyclinA1 expression, regulates CDK2, p53, Bax, cytochrome c, cleaved caspase-3, cleaved PARP, Apaf-1 expression and Bax/Bcl-2 ratio. Cardanol monoene shows weak DPPH radical scavenging activity and AChE inhibition activity. Cardanol monoene is lethal to Artemia salina nauplii. Cardanol monoene. Cardanol monoene can be used for the research of cancer, infection and inflamation .
    Cardanol monoene
  • HY-N2993
    Polyporenic acid C

    		Apoptosis Caspase PARP Akt PTEN MDM-2/p53 JNK Cancer
    Polyporenic acid C is a lanostane-type triterpenoid. Polyporenic acid C can be isolated from Poria cocos. Polyporenic acid C causes the cleavage of caspase-8 and caspase-3, as well as the cleavage of PARP. Polyporenic acid C reduces the phosphorylation level of Akt (Ser473), increases the phosphorylation of PTEN and p53 (Ser15), and activates JNK. Polyporenic acid C induces Apoptosis. Polyporenic acid C shows anticancer activity against non-small cell lung cancer .
    Polyporenic acid C
  • HY-16366
    Briciclib

    ON 014185

    		 Eukaryotic Initiation Factor (eIF) CDK c-Myc MDM-2/p53 Caspase Apoptosis Cancer
    Briciclib (ON 014185) is a eukaryotic translation initiation factor 4E (eIF4E) inhibitor. Briciclib exhibits broad-spectrum anti-cancer activity, including in mantle cell leukemia, breast cancer, gastric cancer, and esophageal cancer cells. Briciclib reduces the expression of cyclin D1 and c-Myc, and enhances the expression of P53 and Cleaved Caspase 3 pro-apoptotic proteins. Briciclib can be used for the study of hematological system tumors and solid tumors .
    Briciclib
  • HY-N0392
    Polygalasaponin F

    		Toll-like Receptor (TLR) PI3K Akt NF-κB MDM-2/p53 Caspase MEK Bcl-2 Family p38 MAPK Mitophagy Reactive Oxygen Species (ROS) Apoptosis Calcium Channel Cardiovascular Disease Infection Neurological Disease
    Polygalasaponin F is an orally active triterpenoid saponin monomer. Polygalasaponin F downregulates the expression of Bax, p53, caspase-3, NF-κB p65 and MEK1; restores and upregulates the expression of Bcl-2; activates the PI3K/Akt signaling pathway; inhibits the phosphorylation of p38 MAPK, nuclear translocation of NF-κB, TLR4-mediated signaling pathway, mitophagy (Mitophagy) and ROS production; enhances cell viability and suppresses apoptosis (Apoptosis). Polygalasaponin F maintains mitochondrial function, alleviates Ca 2+ overload, upregulates pCREB and BDNF, preserves cell viability and inhibits the release of inflammatory cytokines. Polygalasaponin F alleviates lung injury induced by influenza A H1N1 and cerebral ischemia-reperfusion injury. Polygalasaponin F is applicable to researches related to Parkinson's disease, cerebral ischemia, pneumonia induced by influenza A H1N1, stroke and Alzheimer's disease [3] .
    Polygalasaponin F
  • HY-W013105
    Sodium glycocholate hydrate, 98%

    N-Cholylglycine sodium salt, 98%

    		 Bcl-2 Family Caspase Endogenous Metabolite Bacterial MDM-2/p53 P-glycoprotein LPL Receptor FXR G protein-coupled Bile Acid Receptor 1 Apoptosis Others
    Sodium glycocholate hydrate, 98% is a bile acid derivative. Sodium glycocholate hydrate, 98% downregulates MDR1, Bcl-2, MRP1, MRP2 and FXR, upregulates Bax, p53, caspase-9, caspase-3, TGR5 and S1PR2. Sodium glycocholate hydrate, 98% inhibits multidrug resistance and efflux pumps, induces mitochondrial apoptosis, and enhances chemosensitivity. Sodium glycocholate hydrate, 98% modulates related bile acid receptor signaling. Sodium glycocholate hydrate, 98% suppresses growth and conjugation of Enterobacteriaceae and increases their antibiotic susceptibility. Sodium glycocholate hydrate, 98% can be used for the research of colon adenocarcinoma and cholangiocarcinoma (CCA) [3].
    Sodium glycocholate hydrate, 98%
  • HY-N0894
    Octahydrocurcumin
    1 Publications Verification

    Hexahydrobisdemethoxycurcumin

    		 Apoptosis MAP4K NF-κB COX Inflammation/Immunology Cancer
    Octahydrocurcumin (Hexahydrobisdemethoxycurcumin) is an orally active anticancer and anti-inflammatory agent, and is the final hydrogenated metabolite of Curcumin (HY-N0005) in vivo. Octahydrocurcumin exerts its anti-tumor and anti-inflammatory effects by inducing the mitochondrial apoptosis pathway and inhibiting the TAK1-NF-κB-COX-2 pathway, respectively .
    Octahydrocurcumin
  • HY-W075770
    Nickel(II) oxide

    Nickel monoxide

    		 Environmental Pollutants Apoptosis Reactive Oxygen Species (ROS) Caspase TGF-beta/Smad p38 MAPK Akt PI3K Infection Metabolic Disease Cancer
    Nickel(II) oxide (nickel monoxide) is a chemical warfare agent that can enter the body through the respiratory tract and other routes, distributing to organs such as the lungs and testes. The nanoparticle form of nickel(II) oxide (NiO NPs) exhibits antibacterial, anti-leishmanial, anti-diabetic, and anti-cancer activities. NiO NPs can be activated by ultraviolet and visible light, generating reactive oxygen species (ROS). Nickel(II) oxide induces oxidative stress by generating reactive oxygen species, activating the TGF-β1-mediated MAPK and PI3K/AKT pathways, disrupting the MMPs/TIMPs balance, and upregulating the expression of inflammatory factors (IL-1β, IL-6) and apoptosis-related molecules (Bax, caspase-3, p53), while inhibiting the activity of the anti-apoptotic molecule Bcl-2. Nickel(II) oxide induces cytotoxicity, promotes fibrosis, triggers inflammatory responses, and causes apoptosis. Nickel(II) oxide can be applied in research on the safety assessment of nanomaterials, such as in the context of pulmonary fibrosis and reproductive system toxicity [3].
    Nickel(II) oxide
  • HY-N1423B
    Glycocholic acid hydrate
    3 Publications Verification

    		 Endogenous Metabolite Caspase G protein-coupled Bile Acid Receptor 1 LPL Receptor MDM-2/p53 Bcl-2 Family P-glycoprotein FXR Bacterial Apoptosis Metabolic Disease Inflammation/Immunology Cancer
    Glycocholic acid hydrate is a bile acid derivative. Glycocholic acid hydrate downregulates MDR1, Bcl-2, MRP1, MRP2 and FXR, upregulates Bax, p53, caspase-9, caspase-3, TGR5 and S1PR2. Glycocholic acid hydrate inhibits multidrug resistance and efflux pumps, induces mitochondrial apoptosis, and enhances chemosensitivity. Glycocholic acid hydrate modulates related bile acid receptor signaling. Glycocholic acid hydrate suppresses growth and conjugation of Enterobacteriaceae and increases their antibiotic susceptibility. Glycocholic acid hydrate can be used for the research of colon adenocarcinoma and cholangiocarcinoma (CCA) [3].
    Glycocholic acid hydrate
  • HY-113041
    Prostaglandin A2

    PGA2; Medullin

    		 Apoptosis Caspase PARP ERK MDM-2/p53 JNK HSV Infection Cancer
    Prostaglandin A2 (PGA2) is a Cyclopentenone prostaglandin. Prostaglandin A2 induces Caspase-dependent Apoptosis, activates p53. Prostaglandin A2 activates ERK2 and JNK1/SAPK. Prostaglandin A2 shows antiviral activity against HSV-1. Prostaglandin A2 has anti-tumor effects. Prostaglandin A2 can be used for the research of colorectal cancer, colorectal carcinoma, breast carcinoma, and herpetic keratitis [3].
    Prostaglandin A2
  • HY-B2035
    Pretilachlor

    		Herbicide Caspase Cytochrome P450 MDM-2/p53 Interleukin Related Reactive Oxygen Species (ROS) Apoptosis Others
    Pretilachlor is a chloroacetamide herbicide with biological activities including endocrine disruption, oxidative stress induction, apoptosis induction, and immunotoxicity. Pretilachlor exerts its effects by interfering with hormone metabolism, inducing oxidative stress, activating apoptotic pathways, and inhibiting immune functions. Pretilachlor upregulates the transcription of P53, Mdm2, and Bbc3, and increases the activities of Caspase3 and Caspase9; it upregulates the transcription of genes in the HPG/HPT axis and the activity of aromatase; it induces oxidative stress, elevates ROS levels, and upregulates CAT, SOD, and GPX. Pretilachlor downregulates the transcription of CXCL-C1C, IL-1β, and IL-8. Pretilachlor disrupts the normal physiological processes and embryonic development of fish, exhibiting significant toxicity. Pretilachlor can be used in studies related to weeding, environmental pollution, and behavioral toxicity in fish .
    Pretilachlor
  • HY-12455
    Duocarmycin A

    		ADC Payload Antibiotic DNA Alkylator/Crosslinker Apoptosis Caspase Cancer
    Duocarmycin A is an antitumor antibiotic and DNA alkylating agent with broad-spectrum antibacterial activity, which can serve as a payload for synthesizing antibody-drug conjugates (ADCs). Duocarmycin A selectively binds to the AT-rich minor groove of DNA, forms covalent adducts by alkylating the adenine N3 residue, thereby disrupting DNA structure and inhibiting its replication and transcription. Duocarmycin A induces apoptosis, sub-G1 phase accumulation and chromatin condensation, reduces the levels of pro-caspase-3/9, and induces p53-independent p21 expression. Duocarmycin A is widely used in the research of various malignancies, including leukemia, sarcoma, glioblastoma, as well as multiple solid tumor models such as lung cancer, breast cancer, and colorectal cancer [3].
    Duocarmycin A
  • HY-130437
    p-nitro-Pifithrin-α

    		MDM-2/p53 TGF-β Receptor Caspase Infection Metabolic Disease
    p-nitro-Pifithrin-α, a cell-permeable analog of pifithrin-α, is a potent p53 inhibitor. p-nitro-Pifithrin-α suppresses p53-mediated TGF-β1 expression in HK-2 cells. p-nitro-Pifithrin-α inhibits the activation of caspase-3 by Zika virus (ZIKV) strains. p-nitro-Pifithrin-α attenuates steatosis and liver injury in mice fed a high-fat diet [4]. non-alcoholic fatty liver disease [3].
    p-nitro-Pifithrin-α
  • HY-N11591
    Ganoderic acid T

    		Apoptosis DNA/RNA Synthesis Mitochondrial Metabolism Cancer
    Ganoderic acid T is a lanostane triterpenoid. Ganoderic acid T is isolated from Ganoderma lucidum mycelia. Ganoderic acid T induces Mitochondria-mediated Apoptosis and inhibits DNA synthesis. Ganoderic acid T exhibits anticancer activity against cervical cancer, liver cancer and lung cancer .
    Ganoderic acid T
  • HY-114372
    Lycopodine

    		Lipoxygenase Caspase Apoptosis Cancer
    Lycopodine, a pharmacologically important bioactive component derived from Lycopodium clavatumspores, triggers apoptosis by modulating 5-lipoxygenase, and depolarizing mitochondrial membrane potential in refractory prostate cancer cells without modulating p53 activity . Lycopodine inhibits proliferation of HeLa cells through induction of apoptosis via caspase-3 activation .
    Lycopodine
  • HY-B0960S
    Sulfabenzamide-d4

    N-Sulfanilylbenzamide-d4

    		 Bacterial Autophagy Isotope-Labeled Compounds MDM-2/p53 Caspase PARP DNA-PK Akt Infection Cancer
    Sulfabenzamide (N-Sulfanilylbenzamide)-d4 is the deuterium labeled Sulfabenzamide (HY-B0960). Sulfabenzamide is a sulfonamide antibacterial agent. Sulfabenzamide exhibit antibacterial activity against Staphylococcus aureus (ATCC 25923) and Escherichia coli (ATCC 8739). Sulfabenzamide can promote autophagic cell autophagy in breast cancer cells through p53/ DRAM pathway. Sulfabenzamide increases caspase-3 activity, deactivates PARP1 and DNA-PK, downregulates AKT1 and AKT2. Sulfabenzamide can be used for the researches of breast cancer and bacterial infections .
    Sulfabenzamide-d4
  • HY-178036
    ZM484

    		MDM-2/p53 Topoisomerase Bcl-2 Family Caspase Cyclin G-associated Kinase (GAK) Cancer
    ZM484 is a potent dual p53-MDM2/TOP1 inhibitor that exhibits antiproliferative and antitumor activity both in vitro and in vivo. ZM484 effectively upregulates p53 and MDM2 proteins and maintains TOP1 inhibitory activity by the release of camptothecin (CPT) and a potent p53-MDM2 inhibitor. ZM484 induces cell cycle arrest and apoptosis by regulating the expression of key apoptosis- and cycle-related proteins, including caspase-3, Bcl-2, and Cyclin B1. ZM484 can be used for colorectal cancer research .
    ZM484
  • HY-100035
    PT-262

    		ROCK ERK CDK Apoptosis Cancer
    PT-262 is a potent ROCK inhibitor with an IC50 value of around 5 μM. PT-262 induces the loss of mitochondrial membrane potential and elevates the caspase-3 activation and apoptosis. PT-262 inhibits the ERK and CDC2 phosphorylation via a p53-independent pathway. PT-262 blocks cytoskeleton function and cell migration. PT-262 has anti-cancer activity .
    PT-262
  • HY-P3528
    GPR

    		Caspase Apoptosis Neurological Disease
    GPR is a three amino acid peptide. GPR can rescue cultured rat hippocampal neurons from Aβ-induced neuronal death by inhibiting caspase-3/p53 dependent apoptosis. GPR can be used for the research of Alzheimer's disease (AD).
    GPR
  • HY-175034
    Topoisomerase I/II-IN-1

    		Topoisomerase Apoptosis MDM-2/p53 Bcl-2 Family Caspase Cancer
    Topoisomerase I/II-IN-1 is a dual inhibitor of topoisomerase I/II. Topoisomerase I/II-IN-1 induces G2/M arrest and apoptosis in cancer cells by upregulating p53, p21, and Bax mRNA levels, caspase-3 protein levels, and the Bax/Bcl-2 ratio, while downregulating Bcl-2. Topoisomerase I/II-IN-1 is useful in the study of various cancers, including melanoma, renal cancer, colorectal cancer, and breast cancer .
    Topoisomerase I/II-IN-1
  • HY-B0960R
    Sulfabenzamide (Standard)

    N-Sulfanilylbenzamide (Standard)

    		 Reference Standards Bacterial Autophagy MDM-2/p53 Caspase PARP DNA-PK Akt Infection Cancer
    Sulfabenzamide (N-Sulfanilylbenzamide) (Standard) is the analytical standard of Sulfabenzamide (HY-B0960). This product is intended for research and analytical applications. Sulfabenzamide is a sulfonamide antibacterial agent. Sulfabenzamide exhibit antibacterial activity against Staphylococcus aureus (ATCC 25923) and Escherichia coli (ATCC 8739). Sulfabenzamide can promote autophagic cell autophagy in breast cancer cells through p53/ DRAM pathway. Sulfabenzamide increases caspase-3 activity, deactivates PARP1 and DNA-PK, downregulates AKT1 and AKT2. Sulfabenzamide can be used for the researches of breast cancer and bacterial infections .
    Sulfabenzamide (Standard)
  • HY-N1423S1
    Glycocholic acid-d5

    		Isotope-Labeled Compounds P-glycoprotein Bcl-2 Family G protein-coupled Bile Acid Receptor 1 Endogenous Metabolite Bacterial Apoptosis FXR Caspase MDM-2/p53 LPL Receptor Metabolic Disease Cancer
    Glycocholic acid-d5 is the deuterium labeled Glycocholic acid (HY-N1423). Glycocholic acid is a bile acid derivative. Glycocholic acid downregulates MDR1, Bcl-2, MRP1, MRP2 and FXR, upregulates Bax, p53, caspase-9, caspase-3, TGR5 and S1PR2. Glycocholic acid inhibits multidrug resistance and efflux pumps, induces mitochondrial apoptosis, and enhances chemosensitivity. Glycocholic acid modulates related bile acid receptor signaling. Glycocholic acid suppresses growth and conjugation of Enterobacteriaceae and increases their antibiotic susceptibility. Glycocholic acid can be used for the research of colon adenocarcinoma and cholangiocarcinoma (CCA).
    Glycocholic acid-d5
  • HY-146253
    CDK1/2/4-IN-1

    		CDK Apoptosis Bcl-2 Family Caspase Cancer
    CDK1/2/4-IN-1 (compound 3a) is a potent CDK inhibitor with IC50 values of 1.47, 0.78 and 0.87 μM for CDK1, CDK2 and CDK4, respectively. CDK1/2/4-IN-1 arrests cell cycle at G2/M phase and induces apoptosis. CDK1/2/4-IN-1 elevates Bax, caspase-3, P53 levels and decreases Bcl-2 level. CDK1/2/4-IN-1 can be used for cancer research .
    CDK1/2/4-IN-1
  • HY-178942
    EGFR/VEGFR2-IN-9

    		VEGFR EGFR Apoptosis Bcl-2 Family Caspase MDM-2/p53 Cancer
    EGFR/VEGFR2-IN-9 (Compound 9b) is an inhibitor of VEGFR-2 (IC50 = 1.325 μM) and EGFR (IC50 = 1.891 μM). EGFR/VEGFR2-IN-9 significantly inhibits the proliferation of multiple cancer cell lines, particularly leukemia cells. EGFR/VEGFR2-IN-9 upregulates the expression levels of Bax, caspase-3, and p53, while downregulating the expression of Bcl-2. EGFR/VEGFR2-IN-9 induces apoptosis and arrests the cell cycle in the G1 phase. EGFR/VEGFR2-IN-9 can be used to investigate anti-tumor angiogenesis and multi-drug resistant cancers .
    EGFR/VEGFR2-IN-9
  • HY-168443
    HTR2A antagonist 1

    		5-HT Receptor Apoptosis Cancer
    HTR2A antagonist 1 (Compound 15f) is a HTR2A antagonist, with an IC50 of 42.79 nM. HTR2A antagonist 1 induces sub-G1 cell cycle arrest and apoptosis in colorectal cancer cells via the activation of p53/p21/caspase 3 signaling. HTR2A antagonist 1 has good liver microsomal stability. HTR2A antagonist 1 can be used for the research of colorectal cancer .
    HTR2A antagonist 1
  • HY-120339
    STK899704

    		Microtubule/Tubulin FAK MEK ERK MMP Caspase PARP Apoptosis MDM-2/p53 Cancer
    STK899704 is a tubulin polymerization inhibitor. STK899704 exhibits broad-spectrum inhibitory activity against various cancer cell lines with IC50 values ​​ranging from 0.2 to 1.0 μM. STK899704 disrupts the mitotic spindle structure, inducing G2/M phase cell cycle arrest. STK899704 inhibits the migration ability of HT29 cells by downregulating the FAK-MEK-ERK signaling pathway, thereby suppressing the expression and activity of MMP-2 and MMP-9. STK899704 activates caspase-3/7/8/9, leading to PARP cleavage and inducing apoptosis. STK899704 induces cellular senescence through the p53 pathway. STK899704 can be used in research on skin cancer, lung cancer, colon cancer, and other cancers [3].
    STK899704
  • HY-17548
    VMY-1-103

    		Caspase Apoptosis Cancer
    VMY-1-103 is an inhibitor for cyclin/Cdk complex, that arrests the cell cycle at G1 phase. VMY-1-103 reduces mitochondrial membrane potential, induces p53 phosphorylation and and PARP cleavage, activates caspase-3, and thus induces apoptosis in prostate cancer cell LNCaP .
    VMY-1-103
  • HY-168877
    FMP

    		MDM-2/p53 Reactive Oxygen Species (ROS) Apoptosis Caspase PARP Bcl-2 Family Cancer
    FMP is a Platinum(IV) complexe. FMP significantly upregulates the expression of γ-H2AX and p53. FMP increases the production of ROS. FMP markedly upregulates the expressions of Apoptosis-related proteins (DR5, Fas, caspase-8, Cyt-c, caspase-3, cleaved-PARP1, Bax). FMP shows antiproliferative activity against breast cancer .
    FMP
  • HY-175332
    Apoptosis inducer 43

    		Apoptosis Bcl-2 Family Caspase MDM-2/p53 Cancer
    Apoptosis inducer 43 is an apoptosis inducer. Apoptosis inducer 43 can induce apoptosis, SubG0-G1 cell cycle arrest, secondary necrosis, and upregulate caspase-3, p53, and Bax/Bcl-2 expression in HCT116 cells. Apoptosis inducer 43 can inhibit tumor growth in a solid Ehrlich carcinoma (SEC) mouse model. Apoptosis inducer 43 can be used to study cancers such as colon cancer, leukemia, and non-small cell lung cancer .
    Apoptosis inducer 43
  • HY-N2993R
    Polyporenic acid C (Standard)

    		Reference Standards Apoptosis Caspase PARP Akt PTEN MDM-2/p53 JNK Cancer
    Polyporenic acid C (Standard) is an analytical standard of Polyporenic acid C (HY-N2993). This product is intended for research and analytical applications. Polyporenic acid C is a lanostane-type triterpenoid. Polyporenic acid C can be isolated from Poria cocos. Polyporenic acid C causes the cleavage of caspase-8 and caspase-3, as well as the cleavage of PARP. Polyporenic acid C reduces the phosphorylation level of Akt (Ser473), increases the phosphorylation of PTEN and p53 (Ser15), and activates JNK. Polyporenic acid C induces Apoptosis. Polyporenic acid C shows anticancer activity against non-small cell lung cancer .
    Polyporenic acid C (Standard)
  • HY-N1423AR
    Glycocholic acid sodium (Standard)

    		Reference Standards P-glycoprotein Bcl-2 Family G protein-coupled Bile Acid Receptor 1 Bacterial Apoptosis FXR Caspase MDM-2/p53 LPL Receptor Endogenous Metabolite Metabolic Disease Cancer
    Glycocholic acid (sodium) (Standard) is the analytical standard of Glycocholic acid sodium (HY-N1423A). This product is intended for research and analytical applications. Glycocholic acid sodium is a bile acid derivative. Glycocholic acid downregulates MDR1, Bcl-2, MRP1, MRP2 and FXR, upregulates Bax, p53, caspase-9, caspase-3, TGR5 and S1PR2. Glycocholic acid sodium inhibits multidrug resistance and efflux pumps, induces mitochondrial apoptosis, and enhances chemosensitivity. Glycocholic acid sodium modulates related bile acid receptor signaling. Glycocholic acid sodium suppresses growth and conjugation of Enterobacteriaceae and increases their antibiotic susceptibility. Glycocholic acid sodium can be used for the research of colon adenocarcinoma and cholangiocarcinoma (CCA).
    Glycocholic acid sodium (Standard)
  • HY-172393
    TCF4/β-catenin-IN-1

    		β-catenin Apoptosis Caspase MDM-2/p53 Bcl-2 Family Cytochrome P450 Cancer
    TCF4/β-catenin-IN-1 (Compound 8b) is an inhibitor of TCF4/β-catenin, and induces apoptosis. TCF4/β-catenin-IN-1 up-regulates p53, caspase-3, caspase-8, caspase-9 levels and Bax protein expression as well as down-regulates Bcl-2 protein expression. TCF4/β-catenin-IN-1 can inhibit CYP3A4, CYP1A2, CYP2C19, and shows promising cytotoxic activity in cancer cells .
    TCF4/β-catenin-IN-1
  • HY-W710827
    N,N'-Methylenebisacrylamide-d6

    		Isotope-Labeled Compounds Caspase MDM-2/p53 Biochemical Assay Reagents Cardiovascular Disease Endocrinology Cancer
    N,N'-Methylenebisacrylamide-d6 is the deuterium labeled N,N'-Methylenebisacrylamide (HY-D0848). N,N'-Methylenebisacrylamide (Bisacrylamide) is an orally active acrylamide dimer and crosslinker. N,N'-Methylenebisacrylamide increases CYP2E1, P53, cleaved caspase-3. N,N'-Methylenebisacrylamide promotes hepatic cancer. N,N'-Methylenebisacrylamide changes sperm abnormality rate and sperm count. N,N'-Methylenebisacrylamide decreases the number of various cells in the blood as well as induces liver and testicular damage. N,N'-Methylenebisacrylamide is used to prepare polyacrylamide gel [3] .
    N,N'-Methylenebisacrylamide-d6
  • HY-174260
    Neuroprotective agent 11

    		NO Synthase COX Caspase MDM-2/p53 Neurological Disease
    Neuroprotective agent 11 (Compound 1a) is an orally active polyphenol compound with significant protective effects against cerebral ischemia. The main activities of Neuroprotective agent 11 include inhibiting neuronal inflammation and apoptosis, reducing cerebral infarction volume, and improving behavioral symptoms of cerebral ischemic mice. Neuroprotective agent 11 exerts its regulatory mechanism by downregulating the expression of inflammatory factors (iNOS、COX-2) and apoptotic proteins (cleaved-Caspase3, p53). Neuroprotective agent 11 can be used in the study of cerebral ischemia-related diseases (such as ischemic stroke) .
    Neuroprotective agent 11
  • HY-175848
    NSC 850745

    		c-Met/HGFR STAT Apoptosis Akt VEGFR Bcl-2 Family MDM-2/p53 Caspase Cancer
    NSC 850745 is a selective and potent c-Met/STAT3 inhibitor with IC50 values of 210 and 670 nM. NSC 850745 can inhibit cell proliferation, induce G2/M phase arrest and induce apoptosis. NSC 850745 can downregulate AKT-1, VEGF and Bcl-2 expression and upregulate p53, Bax and caspase expression. NSC 850745 can be used for the research of cancer, such as leukemia and colon cancer .
    NSC 850745
  • HY-W754548
    Glycocholic acid-13C2,d4

    		Isotope-Labeled Compounds Endogenous Metabolite P-glycoprotein Bcl-2 Family G protein-coupled Bile Acid Receptor 1 Bacterial Apoptosis FXR Caspase MDM-2/p53 LPL Receptor Metabolic Disease Cancer
    Glycocholic acid- 13C2,d4 is the deuterium labeled and 13C-labeled Glycocholic acid (HY-N1423). Glycocholic acid is a bile acid derivative. Glycocholic acid downregulates MDR1, Bcl-2, MRP1, MRP2 and FXR, upregulates Bax, p53, caspase-9, caspase-3, TGR5 and S1PR2. Glycocholic acid inhibits multidrug resistance and efflux pumps, induces mitochondrial apoptosis, and enhances chemosensitivity. Glycocholic acid modulates related bile acid receptor signaling. Glycocholic acid suppresses growth and conjugation of Enterobacteriaceae and increases their antibiotic susceptibility. Glycocholic acid can be used for the research of colon adenocarcinoma and cholangiocarcinoma (CCA).
    Glycocholic acid-13C2,d4
  • HY-131710
    PDE5-IN-3

    		Phosphodiesterase (PDE) EGFR Wnt Apoptosis Cancer
    PDE5-IN-3 (compound 11j) is a potent PDE5 inhibitor with an IC50 of 1.57 nM. PDE5-IN-3 shows moderate EGFR inhibition with IC50 of 5.827 µM. PDE5-IN-3 significantly inhibits the Wnt/β-catenin pathway (IC50=1286.96 ng/mL). PDE5-IN-3 induces the intrinsic apoptotic mitochondrial pathway in HepG2 cells. PDE5-IN-3 has strong antitumor activity .
    PDE5-IN-3
  • HY-145289
    Antitumor agent-37

    		Apoptosis Cancer
    Antitumor agent-37 possesses potent anti-proliferative and anti-metastasis activities. Antitumor agent-37 induces serious DNA damage and further leads to high expression of γ-H2AX and p53. Antitumor agent-37 promotes apoptosis of tumor cells through mitochondrial apoptotic pathway Bcl-2/Bax/caspase3. Antitumor agent-37 significantly improves immune response through restraining the expression of PD-L1 to increase CD3+ and CD8+ T infiltrating cells in tumor tissues .
    Antitumor agent-37
  • HY-145288
    Antitumor agent-36

    		Apoptosis Cancer
    Antitumor agent-36 possesses potent anti-proliferative and anti-metastasis activities. Antitumor agent-36 induces serious DNA damage and further leads to high expression of γ-H2AX and p53. Antitumor agent-36 promotes apoptosis of tumor cells through mitochondrial apoptotic pathway Bcl-2/Bax/caspase3. Antitumor agent-36 significantly improves immune response through restraining the expression of PD-L1 to increase CD3+ and CD8+ T infiltrating cells in tumor tissues .
    Antitumor agent-36
  • HY-159938
    p38α inhibitor 6

    		p38 MAPK Apoptosis Bcl-2 Family MDM-2/p53 Caspase Cancer
    p38α inhibitor 6 (compound 19) is a p38α inhibitor with the IC50 of 0.68 μM. p38α inhibitor 6 induces cell apoptosis and arrests cell cycle at G0 and G2/M phase. p38α inhibitor 6 decreases the TNF-α concentration as well as increased the expression of tumor suppressor gene p53, Bax/BCL-2 ratio and caspase 3/7 .
    p38α inhibitor 6
  • HY-N0392R
    Polygalasaponin F (Standard)

    		Reference Standards Toll-like Receptor (TLR) PI3K Akt NF-κB Inflammation/Immunology Cancer
    Polygalasaponin F (Standard) is the analytical standard of Polygalasaponin F. This product is intended for research and analytical applications. Polygalasaponin F is an orally active triterpenoid saponin monomer. Polygalasaponin F downregulates the expression of Bax, p53, caspase-3, NF-κB p65 and MEK1; restores and upregulates the expression of Bcl-2; activates the PI3K/Akt signaling pathway; inhibits the phosphorylation of p38 MAPK, nuclear translocation of NF-κB, TLR4-mediated signaling pathway, mitophagy (Mitophagy) and ROS production; enhances cell viability and suppresses apoptosis (Apoptosis). Polygalasaponin F maintains mitochondrial function, alleviates Ca 2+ overload, upregulates pCREB and BDNF, preserves cell viability and inhibits the release of inflammatory cytokines. Polygalasaponin F alleviates lung injury induced by influenza A H1N1 and cerebral ischemia-reperfusion injury. Polygalasaponin F is applicable to researches related to Parkinson's disease, cerebral ischemia, pneumonia induced by influenza A H1N1, stroke and Alzheimer's disease.
    Polygalasaponin F (Standard)

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