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Pathways Recommended: MAPK/ERK Pathway
Results for "

caspase-3 pathway

" in MedChemExpress (MCE) Product Catalog:

151

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1

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8

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1

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48

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4

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3

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Targets Recommended:
Cat. No. Product Name Target Research Areas Chemical Structure
  • 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 .
    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 .
    Beta-Sitosterol (purity>80%)
  • HY-10805
    Almorexant
    5+ Cited Publications

    ACT 078573

    		 Orexin Receptor (OX Receptor) Calcium Channel Caspase Apoptosis Neurological Disease Endocrinology Cancer
    Almorexant (ACT 078573) is an orally active, potent and competitive dual orexin receptor antagonist, with Kd values of 1.3 nM (OX1) and 0.17 nM (OX2), respectively. Almorexant reversibly blocks signaling of orexin-A and orexin-B peptides. Almorexant totally blocked the intracellular Ca 2+ signal pathway. Almorexant stimulates caspase-3 activity in AsPC-1 cells and induces apoptosis .
    Almorexant
  • HY-126741
    Azadirachtin
    2 Publications Verification

    		 Environmental Pollutants Parasite Caspase NF-κB Apoptosis Bcl-2 Family Infection Inflammation/Immunology Cancer
    Azadirachtin is an oral active triterpenoid compound with anticancer, antimalarial, anti-inflammatory, and insecticidal activities. Azadirachtin induces cell apoptosis through the mitochondrial pathway (by inhibiting Bcl-2/Bax ratio or activating Apaf-1 and caspase-3) or through death receptors (by inhibiting TNFR activation). Additionally, Azadirachtin exerts its anti-inflammatory effects by inhibiting NF-кB signaling pathway activation, and it exhibits insecticidal activity by inducing apoptosis in insect cells .
    Azadirachtin
  • HY-164388
    Z-VAD
    15+ Cited Publications

    		 Caspase Apoptosis Autophagy Necroptosis Cardiovascular Disease Cancer
    Z-VAD is an irreversible, broad-spectrum pan-caspase inhibitor that can inhibit a variety of caspases including caspase-3, -6, -7, -8, -9, etc. (with a weaker inhibitory effect on caspase-2). Z-VAD can block apoptosis signaling pathways, induce autophagy and necrosis in tumor cells, and has anti-angiogenic activity. Z-VAD can enhance the sensitivity of breast cancer and lung cancer cells to radiotherapy in vitro and in vivo, and prolong the growth delay of tumor xenograft models. Z-VAD is well tolerated and is mainly used in research related to cancer radiosensitization and cell death pathway regulation .
    Z-VAD
  • HY-121320
    Raptinal
    5+ Cited Publications

    		 Caspase Apoptosis Cancer
    Raptinal, a agent that directly activates caspase-3, initiates intrinsic pathway caspase-dependent apoptosis. Raptinal is able to rapidly induce cancer cell death by directly activating the effector caspase-3, bypassing the activation of initiator caspase-8 and caspase-9 .
    Raptinal
  • HY-N0576
    Solanesol
    2 Publications Verification

    		 Endogenous Metabolite Heme Oxygenase (HO) HSP p38 MAPK Akt Apoptosis Caspase PARP Neurological Disease Metabolic Disease Inflammation/Immunology
    Solanesol is an orally active aliphatic terpene alcohol. Solanesol is mainly found in tobacco and other Solanaceae plants. Solanesol induces HO-1 and Hsp70 expression, activates p38 and Akt signaling pathways, and inhibits Apoptosis (reduces caspase-3 and PARP cleavage). Solanesol has antioxidant, anti-inflammatory, and neuroprotective activities. Solanesol can be used in the research of Huntington's disease, alcoholic liver disease, chronic inflammatory pain, anxiety, Alzheimer's disease, and bipolar disorder .
    Solanesol
  • HY-B1839
    Fluazinam

    		Environmental Pollutants JNK Fungal p38 MAPK Bcl-2 Family Caspase Autophagy Apoptosis Infection
    Fluazinam is an orally active dinitroaniline fungicide. Fluazinam induces phosphorylation of JNK, activates p38 pathway, decreases Bcl-2, activates caspase-3, decreases complex I activity, increases Autophagy and Apoptosis. Fluazinam has strong antifungal activity against F. fujikuroi and B. maydis. Fluazinam has a negative impact on Brachydanio rerio and worker bees .
    Fluazinam
  • HY-N0763
    Angelicin
    10+ Cited Publications

    Isopsoralen

    		 Apoptosis Virus Protease NF-κB p38 MAPK JNK Caspase Infection Inflammation/Immunology Cancer
    Angelicin is a furanocoumarin compound that functions as an inhibitor of NF-κB and MAPK signaling pathways, exhibiting anti-inflammatory, antiviral, and antitumor activities. It suppresses the lytic replication of γ-herpesviruses, such as MHV-68, early during viral infection, potentially inhibiting RTA gene expression (IC50=28.95 μM). Angelicin also mitigates inflammation by inhibiting the phosphorylation and nuclear translocation of NF-κB, and the phosphorylation of p38 and JNK. Furthermore, it induces apoptosis in neuroblastoma cells by downregulating anti-apoptotic proteins like Bcl-2, Bcl-xL, and Mcl-1, while activating caspase-9 and caspase-3.
    Angelicin
  • HY-N0732
    Jolkinolide B
    1 Publications Verification

    		 IAP Akt Caspase NF-κB TGF-beta/Smad JAK Bacterial Apoptosis Infection Metabolic Disease Inflammation/Immunology Cancer
    Jolkinolide B is a bioactive diterpene isolated from the roots of Euphorbia fischeriana Steud with oral activity. Jolkinolide B downregulates XIAP, cIAP1, cIAP2, and phosphorylated Akt, upregulates Smac, activates caspase-3 and caspase-9, and inhibits NF-κB, TGFβ/smad3 and JAK/STAT3 pathways. Jolkinolide B exerts comprehensive biological effects including inducing cancer cell apoptosis, suppressing inflammatory responses, improving lung function, alleviating hepatic steatosis and eliminating intracellular Mycobacterium tuberculosis. Jolkinolide B can be used for the research of leukemia, histiocytic lymphoma, asthma, metabolic dysfunction-associated steatotic liver disease and tuberculosis .
    Jolkinolide B
  • HY-N0712
    Typhaneoside
    3 Publications Verification

    		 Autophagy mTOR Akt FXR Cardiovascular Disease Neurological Disease Metabolic Disease Cancer
    Typhaneoside is an orally bioavailable signal modulator and cellular regulator. Typhaneoside regulates the PI3K/Akt/mTOR autophagy transduction pathway. Typhaneoside promotes the activation of AMP-activated protein kinase and Caspase-3, induces apoptosis, ferroptosis, autophagy, ROS accumulation, and cell cycle arrest at the G2/M phase, and reduces cancer cell viability. Typhaneoside activates the farnesoid X receptor signaling pathway, improves glucose and lipid metabolism, alleviates inflammatory responses, oxidative stress and hepatic lipid accumulation, and exerts hepatoprotective effects. Typhaneoside is applicable to research related to post-myocardial infarction heart failure, acute myeloid leukemia, non-alcoholic fatty liver disease, and neurological disorders .
    Typhaneoside
  • HY-137371
    Lactonic sophorolipid

    		Bacterial Apoptosis Antibiotic Infection Cancer
    Lactonic sophorolipid is an apoptosis inducer and antimicrobial surfactant with antitumor activity. Lactonic sophorolipid regulates Bax/Bcl-gene expression through caspase-3/9 and induces apoptosis in tumor cells. Lactonic sophorolipid can disrupt cell membrane permeability and exert antibacterial effects (MIC for oral pathogens is 100-400 μg/mL). Lactonic sophorolipid promotes mitochondrial membrane potential depolarization, activates the intrinsic apoptotic pathway, and can synergize with antibiotics to enhance the antibacterial effect. Lactonic sophorolipid can be used in liver cancer research and the development of oral hygiene antibacterial agents[1][2][3].
    Lactonic sophorolipid
  • HY-10805A
    Almorexant hydrochloride
    5+ Cited Publications

    ACT 078573 hydrochloride

    		 Orexin Receptor (OX Receptor) Calcium Channel Caspase Apoptosis Neurological Disease Endocrinology Cancer
    Almorexant (ACT 078573) hydrochloride is an orally active, potent and competitive dual orexin receptor antagonist, with Kd values of 1.3 nM (OX1) and 0.17 nM (OX2), respectively. Almorexant hydrochloride reversibly blocks signaling of orexin-A and orexin-B peptides. Almorexant hydrochloride totally blocked the intracellular Ca 2+ signal pathway. Almorexant hydrochloride stimulates caspase-3 activity in AsPC-1 cells and induces apoptosis .
    Almorexant hydrochloride
  • HY-B0347
    Lacidipine
    2 Publications Verification

    		 Calcium Channel Reactive Oxygen Species (ROS) Caspase Apoptosis Cardiovascular Disease
    Lacidipine is an orally active and highly selective L-type calcium channel blocker that acts on smooth muscle calcium channels, primarily dilates peripheral arteries, reduces peripheral resistance, and has long-lasting anti-hypertensive activity. Lacidipine protects HKCs from apoptosis induced by ATP depletion and recovery by modulating the caspase-3 pathway. Lacidipine can be used in studies of hypertension, atherosclerosis and acute kidney injury (AKI) .
    Lacidipine
  • HY-N11908
    α-Santalol

    cis-α-Santalol

    		 Akt Survivin Apoptosis Caspase PARP Metabolic Disease Cancer
    α-Santalol (cis-α-Santalol), a naturally occurring sesquiterpene, is an orally active anticancer agent and apoptosis inducer. α-Santalol activates caspase-3 to drive apoptotic processes. >α-Santalol induces apoptosis, decreases cell viability, and causes PARP cleavage in human prostate cancer cells. α-santalol inhibits Akt/Survivin pathway to induce cell death. α-Santalol can be used for the research of prostate cancer and diabetes mellitus .
    α-Santalol
  • HY-P10102
    Kp7-6
    2 Publications Verification

    		 Apoptosis PERK NF-κB Caspase JNK Inflammation/Immunology Cancer
    Kp7-6 is a Fas mimetic peptide and also a Fas/FasL antagonist. Kp7-6 specifically binds to Fas and FasL, disrupts receptor complexes, and blocks downstream apoptosis signaling pathways. Kp7-6 inhibits the phosphorylation of ERK1-2, induces the phosphorylation of IκBα, and activates NF-κB. Kp7-6 inhibits the activation of caspase-8, caspase-3 and JNK, and suppresses human amylin-induced β-cell apoptosis. Kp7-6 inhibits FasL-induced lymphoid cytotoxicity and apoptosis. Kp7-6 reduces local tumor FasL expression, increases CD8 +Fas + T cell infiltration, and decreases tumor volume in pancreatic neuroendocrine tumor models. Kp7-6 prevents concanavalin A-induced liver injury in mice. Kp7-6 is applicable to research related to type 2 diabetes, concanavalin A-induced hepatitis and pancreatic neuroendocrine tumors .
    Kp7-6
  • HY-N2877
    Annonacin
    1 Publications Verification

    		 Potassium Channel Sodium Channel Na+/K+ ATPase Calcium Channel Apoptosis Neurological Disease Cancer
    Annonacin is an acetylgenin that is toxic by inhibiting the pathway of the mitochondrial complex. Annonacin increases tau phosphorylation in R406W +/+ mice. Annonacin acts as an inhibitor of the sodium/potassium and sarcoplasmic reticulum (SERCA) ATPase pumps. Annonacin has significant killing effect on ovarian cancer cell, cervical cancer cell, breast cancer cell, bladder cancer cell and skin cancer cell. Annonacin induces apoptosis through Bax and Caspase-3-related pathways .
    Annonacin
  • HY-N0660
    Jujuboside B

    		Apoptosis PARP Caspase AMPK Autophagy VEGFR Keap1-Nrf2 STING 11β-HSD Ferroptosis PI3K Akt p38 MAPK ERK Neurological Disease Metabolic Disease Inflammation/Immunology Cancer
    Jujuboside B is a bioactive saponin component isolated from Ziziphi Spinosae Semen (sour jujube seed), with oral efficacy and blood-brain barrier permeability. Jujuboside B induces acute leukemia cell death and drives necroptosis apoptosis by activating the RIPK1/RIPK3/MLKL pathway. Jujuboside B upregulates the expression of NOXA, PARP and caspase-3, activates AMPK, inhibits the proliferation of breast cancer cells, and induces cell apoptosis and autophagy. Jujuboside B inhibits angiogenesis and tumor growth by blocking the VEGFR-2 signaling pathway. Jujuboside B alleviates liver injury in mice by regulating the Nrf2-STING signaling pathway . Jujuboside B alleviates liver injury by regulating anti-inflammatory responses and downregulating the expression of 11β-HSD2. Jujuboside B induces ferroptosis and overcomes radioresistance in non-small cell lung cancer via the PPARγ-ATF3-Gpx4 signaling pathway. Jujuboside B exerts inhibitory effects on platelet aggregation. Jujuboside B inhibits febrile seizures by suppressing the activity of AMPA receptors. Jujuboside B reverses chronic unpredictable mild stress-promoted tumor progression by blocking the PI3K/Akt and MAPK/ERK pathways and dephosphorylating CREB signaling. Jujuboside B is applicable to related studies on acute leukemia, breast cancer, PM2.5-induced lung injury, hepatotoxicity, liver injury, colorectal cancer, non-small cell lung cancer, thromboembolic diseases, cardiovascular diseases associated with high platelet aggregation, febrile seizures, and depressive-like phenotypes .
    Jujuboside B
  • 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-N3376
    Liriodenine

    Spermatheridine; VLT045

    		 Apoptosis Cancer
    Liriodenine (Spermatheridine; VLT045) is an aporphine alkaloid isolated from the plant?Mitrephora sirikitiae?and has anti-cancer activities . Liriodenine induces cell apoptosis, activates the intrinsic pathway by induction of caspase-3 and caspase-9 .
    Liriodenine
  • HY-B0877
    Halcinonide
    1 Publications Verification

    SQ-18566

    		 Smo Caspase RAR/RXR CDK Cardiovascular Disease Neurological Disease Inflammation/Immunology
    Halcinonide (SQ-18566) is an orally active Smoothened (Smo) agonist. Halcinonide activates the Hedgehog signaling pathway by binding to Smo and promoting its internalization and expression, thereby activating Gli transcription factors. Halcinonide not only stimulates cell proliferation, increases the expression of cyclin D2/CDK6 and inhibits the degradation of caspase-3, but also suppresses Bcl-2/Bax-mediated apoptosis, oxidative stress and inflammatory responses. Halcinonide activates RxRγ to upregulate the expression of myelin genes, thereby reducing cerebral infarction and improving behavioral deficits. Halcinonide has been used in studies related to multiple sclerosis and ischemic stroke .
    Halcinonide
  • HY-172209
    PPIA-IN-1

    		p38 MAPK Apoptosis Reactive Oxygen Species (ROS) Caspase Bcl-2 Family Cancer
    PPIA-IN-1 is a PPIA inhibitor with a Kd value of 0.52 μM. PPIA-IN-1 inhibits the PPIA/MAPK signaling pathway to exert antiproliferative activity. PPIA-IN-1 induces G0/G1 cell cycle arrest in cancer cells. PPIA-IN-1 upregulates the expression of Bax and caspase-3, downregulates Bcl-2 expression, and induces apoptosis in cancer cells. PPIA-IN-1 induces increased ROS levels, DNA damage, endoplasmic reticulum stress, and mitochondrial dysfunction in cancer cells. PPIA-IN-1 exhibits antitumor activity in a mouse colon cancer xenograft model. PPIA-IN-1 can be used for the research of colorectal cancer .
    PPIA-IN-1
  • HY-N1983
    Caudatin
    1 Publications Verification

    		 Apoptosis Autophagy Reactive Oxygen Species (ROS) Mitochondrial Metabolism PARP Caspase Bcl-2 Family VEGFR FAK WDR5 p38 MAPK JNK PPAR Neurological Disease Inflammation/Immunology Cancer
    Caudatin is an orally active and brain-penetrant C-21 steroidal found in Cynanchum bungei decne with a variety of biological activities. Caudatin can inhibit cell proliferation, migration, invasion, cause cell phase arrest, induce apoptosis, autophagy, ROS prodution and loss of mitochondrial membrane potential. Caudatin activates PARP, caspase-3, -7, -9, upregulates pro-apoptotic Bad and Bax and downregulates anti-apoptotic Bcl-2 and Bcl-XL. Caudatin suppresses VEGF, FAK phosphorylation, upregulates p21, p27, DR5 protein expression, activates the p38 MAPK, JNK and PPARα/TFEB-mediated autophagy-lysosomal signaling pathways. Caudatin can be used for the research of cancer, inflammation and neurological disease, such as glioma and Alzheimer's disease .
    Caudatin
  • 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 .
    Polygalasaponin F
  • HY-160229
    ssRNA40 sodium

    R-1075 sodium

    		 Toll-like Receptor (TLR) MyD88 Caspase Reactive Oxygen Species (ROS) Autophagy Pyroptosis HIV Infection Neurological Disease
    ssRNA40 sodium (R-1075 sodium) is a single-stranded RNA40 derived from HIV-1. ssRNA40 sodium activates the TLR7, TLR8, TLR2, RIG-I, MDA5, MyD88, Caspase-3, IRE1α, NLRP3 inflammasome and IRF7 signaling pathways. ssRNA40 sodium alters mRNA expression in neutrophils, induces pro-inflammatory cytokines, ROS, autophagy (autophagy), pyroptosis (pyroptosis), neuronal death, neurodegeneration, aggregate formation and NK cell activation. ssRNA40 sodium activates the expression of CD62L, CD11b, CD69, MX1, OAS1, ATG7, LC3B and XBP1 in immune cell and neuronal populations. ssRNA40 sodium causes cortical neuron loss and axonal damage in mice in a TLR7-dependent manner. ssRNA40 sodium can be used in research on HIV-1 infection, neurodegeneration, COVID-19 and HIV-associated neurological disorders .
    ssRNA40 sodium
  • HY-176761
    NSC647889

    		Apoptosis Autophagy Caspase mTOR Cancer
    NSC647889 is an apoptosis and autophagy inducer. NSC647889 induces apoptosis, inhibits mTOR pathway and abrogates DNA synthesis. NSC647889 triggers LC3-positive vesicle formation, modulates AKT and 4EBP1 phosphorylation and shows heightened caspase-3 activation in multicellular spheroids. NSC647889 can be used for the research of solid cancer tumour, head-neck carcinoma, and colorectal cancer .
    NSC647889
  • HY-N6801
    Nivalenol

    		Caspase Apoptosis Bcl-2 Family Infection Inflammation/Immunology Cancer
    Nivalenol, a trichothecene mycotoxin that can be produced by Fusarium graminearum, is a fungal metabolite present in agricultural product. Nivalenol modulates apoptotic pathway, cell cycle regulation, Bax, ERK, caspase-3, and poly-ADP-ribose synthase activity in macrophages. Nivalenol inhibits ribosomal peptidyltransferase site, protein synthesis, DNA synthesis, and cell proliferation. Nivalenol induces late-stage apoptotic morphological changes, reduces cellular metabolism, and decreases cell proliferation in erythroleukemia cells. Nivalenol induces lymphocyte apoptosis in murine thymus, spleen, and Peyer's patches. Nivalenol can be used for the research of erythroleukemia .
    Nivalenol
  • HY-15472
    PRX-08066

    		5-HT Receptor p38 MAPK TGF-β Receptor FGFR Apoptosis Caspase Cardiovascular Disease Neurological Disease Cancer
    PRX-08066 is a selective and orally active 5-hydroxytryptamine receptor 2B (5-HT2BR) antagonist with a Ki of 3.4 nM. PRX-08066 inhibits the MAPK pathway, 5-HT release and fibrotic factor (TGFβ1, CTGF and FGF2) expression. PRX-08066 inhibits the proliferation of KRJ-I cells and induces apoptosis (caspase-3 activation). PRX-08066 inhibits pulmonary vascular remodeling. PRX-08066 can be used of pulmonary Arterial Hypertension (PAH) and neuroendocrine tumor (NET) .
    PRX-08066
  • HY-11095
    NPS 2390

    		mGluR CaSR PI3K Akt mTOR Autophagy Apoptosis Bcl-2 Family Caspase Cardiovascular Disease Neurological Disease
    NPS 2390 is an allosteric antagonist of calcium-sensing receptor (CaSR) and mGluR1/5. NPS 2390 inhibits the PI3K/Akt/mTOR signaling pathway, reduces hypoxia-induced intracellular calcium elevation, decreases the expression of autophagy (autophagy) proteins, regulates the expression of phenotypic marker proteins, and inhibits the proliferation of pulmonary artery smooth muscle cells. NPS 2390 attenuates the endogenous apoptosis (apoptosis) pathway, increases the expression level of Bcl-2, downregulates the expression levels of Bax, cytochrome c and caspase-3, alleviates cerebral edema and improves neurological function in rat models. NPS 2390 can be used in studies related to hypoxic pulmonary hypertension, traumatic brain injury, stroke and pain .
    NPS 2390
  • HY-N0566
    23-Hydroxybetulinic acid

    Anemosapogenin

    		 Apoptosis Autophagy Bcl-2 Family Caspase Survivin p38 MAPK MMP Cancer
    23-Hydroxybetulinic acid (Anemosapogenin) is an orally active triterpenoid with broad-spectrum anticancer activity. 23-Hydroxybetulinic acid reduces the levels of Bcl-2 and survivin, elevates the level of Bax, promotes the cleavage/activation of caspase-3 and caspase-9, and induces apoptosis via the endogenous mitochondrial pathway involving cytochrome C release and mitochondrial membrane potential disruption. 23-Hydroxybetulinic acid arrests the cell cycle at S and G1 phases, inhibits cancer cell proliferation, blocks the MAPK signaling pathway, regulates MMP2, and induces autophagic apoptosis by upregulating beclin-1. 23-Hydroxybetulinic acid inhibits the activity and efflux function of P-gp, increases the intracellular accumulation of chemotherapeutic drugs, and synergistically enhances cytotoxicity with Doxorubicin (HY-15142). 23-Hydroxybetulinic acid inhibits the phosphorylation and nuclear translocation of STAT6, blocks M2 macrophage polarization, and reduces M2 macrophage-mediated apoptosis resistance of colon cancer cells. 23-Hydroxybetulinic acid can be used in related studies on chronic myeloid leukemia, hepatocellular carcinoma, sarcoma 180, multidrug-resistant breast cancer, leukemia, Doxorubicin-induced cardiotoxicity, and colorectal cancer .
    23-Hydroxybetulinic acid
  • 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 .
    Nickel(II) oxide
  • HY-W017424
    2-Aminobenzothiazole

    		Drug Intermediate Caspase Apoptosis Neurological Disease Cancer
    2-Aminobenzothiazole acts as a caspase 3/7 activator, an anticancer cytotoxic agent, and also exhibits neurotoxicity. 2-Aminobenzothiazole drives the apoptotic pathway by activating caspase 3/7, induces mitochondrial inner membrane depolarization, and triggers both early and late apoptosis via a caspase-dependent pathway. In zebrafish models, 2-Aminobenzothiazole induces oxidative damage in brain tissues and inhibits genes related to GABA and 5-HT synthesis pathways. Long-term exposure to 2-Aminobenzothiazole impairs motor ability, social behavior, anxiety-like state and cognitive function. 2-Aminobenzothiazole can be used in studies of human laryngeal carcinoma and related neurotoxicity .
    2-Aminobenzothiazole
  • HY-P10939A
    Ac-DMLD-CMK TFA

    		Caspase Pyroptosis Inflammation/Immunology Cancer
    Ac-DMLD-CMK TFA is a caspase 3 inhibitor and a GSDME inhibitor. Ac-DMLD-CMK TFA binds directly to the catalytic domain of caspase-3, blocks caspase-3-mediated cleavage of GSDME, inhibits the activation of caspase 3 and Gsdme in the caspase 3-Gsdme signaling pathway, and reduces the levels of pyroptosis and apoptosis as well as the expression of LDH, IL-6, IL-1β and IL-18. Ac-DMLD-CMK TFA alleviates renal function deterioration, renal tubular epithelial cell injury, inflammatory cytokine secretion, pulmonary structural damage, and chemotherapy-induced nephrotoxicity .
    Ac-DMLD-CMK TFA
  • HY-N5073
    Vitexin-4''-O-glucoside

    4''-O-Glucosylvitexin

    		 JNK p38 MAPK Interleukin Related TNF Receptor Caspase Lactate Dehydrogenase Apoptosis Cardiovascular Disease Metabolic Disease
    Vitexin-4''-O-glucoside (4''-O-Glucosylvitexin) is an orally active natural flavonoid component with multiple pharmacological effects including antioxidation, anti-inflammation, cytoprotection and anti-apoptosis. Vitexin-4''-O-glucoside regulates the MAPK signaling pathway by downregulating the phosphorylation levels of JNK and p38, thereby blocking endoplasmic reticulum stress responses. Vitexin-4''-O-glucoside alleviates oxidative stress by reducing MDA content and upregulating the activities of SOD and CAT, attenuates inflammation by downregulating the expressions of inflammatory factors TNF-α, IL-1β and IL-6, and also reduces LDH release and inhibits caspase-3 activation. Vitexin-4''-O-glucoside effectively improves drug-induced acute liver injury and exerts significant protective effects against myocardial hypoxia/reoxygenation injury. Vitexin-4''-O-glucoside can be used in studies on acute liver injury, cardiovascular diseases and myocardial hypoxia-reoxygenation injury .
    Vitexin-4''-O-glucoside
  • HY-P10939
    Ac-DMLD-CMK

    		Caspase Pyroptosis Inflammation/Immunology Cancer
    Ac-DmLD-CMK is a caspase 3 inhibitor and a GSDME inhibitor. Ac-DmLD-CMK binds directly to the catalytic domain of caspase-3, blocks caspase-3-mediated cleavage of GSDME, inhibits the activation of caspase 3 and Gsdme in the caspase 3-Gsdme signaling pathway, and reduces the levels of pyroptosis and apoptosis as well as the expression of LDH, IL-6, IL-1β and IL-18. Ac-DmLD-CMK alleviates renal function deterioration, renal tubular epithelial cell injury, inflammatory cytokine secretion, pulmonary structural damage, and chemotherapy-induced nephrotoxicity .
    Ac-DMLD-CMK
  • HY-B1839R
    Fluazinam (Standard)

    		Reference Standards Fungal JNK p38 MAPK Bcl-2 Family Caspase Autophagy Apoptosis Infection
    Fluazinam (Standard) is the analytical standard of Fluazinam (HY-B1839). This product is intended for research and analytical applications. Fluazinam is a broad spectrum pyridinamine fungal inhibitor. Fluazinam is an orally active dinitroaniline fungicide. Fluazinam induces phosphorylation of JNK, activates p38 pathway, decreases Bcl-2, activates caspase-3, decreases complex I activity, increases Autophagy and Apoptosis. Fluazinam has strong antifungal activity against F. fujikuroi and B. maydis. Fluazinam has a negative impact on Brachydanio rerio and worker bees .
    Fluazinam (Standard)
  • HY-N12378
    β-Patchoulene

    		NF-κB Toll-like Receptor (TLR) PKA Epigenetic Reader Domain Keap1-Nrf2 Sirtuin AMPK Caspase FASTK ERK ROCK Apoptosis Metabolic Disease Inflammation/Immunology Cancer
    β-Patchoulene is an orally active anti-inflammatory, antioxidant, and anti-apoptotic agent. β-Patchoulene inhibits the NF-κB, TLR4, and cAMP/PKA/CREB signaling pathways; activates the Sirt1/Nrf2 and AMPK signaling pathways; and targets Fas/FasL, Caspase-3, ERK1/2, ROCK1/MLC2 for inhibition. β-Patchoulene regulates cytokine secretion, inflammatory cell infiltration, lipid peroxidation, cell polarization, gut microbiota, and lipid metabolism, restores barrier function, mitochondrial function, and cell viability, and exhibits repellent activity against Spodoptera exigua larvae. β-Patchoulene can be used in research related to various inflammatory, ischemic, fibrosis-associated diseases, as well as hepatocellular carcinoma .
    β-Patchoulene
  • HY-147929
    Apoptotic agent-3

    		Apoptosis Caspase Bcl-2 Family Cancer
    Apoptotic agent-3 (compound 15f) promotes apoptosis through the potential mitochondria-mediated Bcl-2/Bax pathway and activation of the Caspase 3 pathway. Apoptotic agent-3 exhibits anti-proliferative activities and can be used for cancer research .
    Apoptotic agent-3
  • HY-N6690
    Destruxin B
    1 Publications Verification

    		 Bcl-2 Family Caspase Apoptosis Infection Cancer
    Destruxin B, isolated from entomopathogenic fungus Metarhizium anisopliae, is one of the cyclodepsipeptides with insecticidal and anticancer activities. Destruxin B induces apoptosis via a Bcl-2 Family-dependent mitochondrial pathway in human nonsmall cell lung cancer cells . Destruxin B significantly activates caspase-3 and reduces tumor cell proliferation through caspase-mediated apoptosis, not only in vitro but also in vivo .
    Destruxin B
  • HY-N6801S
    Nivalenol-13C15

    		Isotope-Labeled Compounds Caspase Apoptosis Bcl-2 Family Infection Inflammation/Immunology Cancer
    Nivalenol- 13C15 is the 13C labeled Nivalenol (HY-N6801) . Nivalenol, a trichothecene mycotoxin that can be produced by Fusarium graminearum, is a fungal metabolite present in agricultural product. Nivalenol modulates apoptotic pathway, cell cycle regulation, Bax, ERK, caspase-3, and poly-ADP-ribose synthase activity in macrophages. Nivalenol inhibits ribosomal peptidyltransferase site, protein synthesis, DNA synthesis, and cell proliferation. Nivalenol induces late-stage apoptotic morphological changes, reduces cellular metabolism, and decreases cell proliferation in erythroleukemia cells. Nivalenol induces lymphocyte apoptosis in murine thymus, spleen, and Peyer's patches. Nivalenol can be used for the research of erythroleukemia.
    Nivalenol-13C15
  • HY-N2490
    Dehydrotrametenolic acid

    		Caspase Apoptosis Inflammation/Immunology Cancer
    Dehydrotrametenolic acid is a sterol isolated from the sclerotium of Poria cocos. Dehydrotrametenolic acid induces apoptosis through caspase-3 pathway. Dehydrotrametenolic acid has anti-tumor activity, anti-inflammatory, anti-diabetic effects .
    Dehydrotrametenolic acid
  • HY-136778
    INH2BP

    		PARP Reactive Oxygen Species (ROS) Bcl-2 Family Caspase ERK p38 MAPK Cardiovascular Disease
    INH2BP is a poly(ADP-ribose) polymerase (PARP) inhibitor with antioxidant and anti-apoptotic activities. INH2BP reduces the production of intracellular reactive oxygen species (ROS), modulates the expression of apoptosis-related proteins such as Bax, Bcl-2 and cleaved caspase-3 and enhances cell survival through the activation of the ERK1/2 and p38 MAPK signaling pathways. INH2BP is promising for research of cardiovascular diseases .
    INH2BP
  • HY-B0347S1
    Lacidipine-13C8

    		Apoptosis Caspase Calcium Channel Reactive Oxygen Species (ROS) Cardiovascular Disease
    Lacidipine- 13C8 is the deuterium labeled Lacidipine . Lacidipine is an orally active and highly selective L-type calcium channel blocker that acts on smooth muscle calcium channels, primarily dilates peripheral arteries, reduces peripheral resistance, and has long-lasting anti-hypertensive activity. Lacidipine protects HKCs from apoptosis induced by ATP depletion and recovery by modulating the caspase-3 pathway. Lacidipine can be used in studies of hypertension, atherosclerosis and acute kidney injury (AKI) .
    Lacidipine-13C8
  • 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-175700
    YCJ-02

    		Topoisomerase Apoptosis Cancer
    YCJ-02 is a selective Topoisomerase I (Top I) inhibitor. YCJ-02 can inhibit cell proliferation and induce apoptosis and G2/M phase arrest. YCJ-02 can induce DNA damage and increaseγ-H2AX levels. YCJ-02 can promote Top I deqradation via a ubiquitin/26S proteasome pathway. YCJ-02 increases the expressions of pro-apoptotic proteins Bad, Bax, and cleaved caspase-3. YCJ-02 shows broad-spectrum antitumor activity. YCJ-02 can be used for the research of cancer, such as intrahepatic cholangiocarcinoma (ICC) .
    YCJ-02
  • HY-175548
    Nrf2 activator-21

    		Keap1-Nrf2 Apoptosis Caspase Neurological Disease
    Nrf2 activator-21 is a Nrf2 activator with dual antioxidant and neuroprotective properties. Nrf2 activator-21 binds to Keap1 Kelch domain and disrupts Keap1-Nrf2 interactions and activate antioxidant defense mechanisms. Nrf2 activator-21 reduces apoptosis and decreases caspase-3 activity in the hippocampal neurons. Nrf2 activator-21 targets cerebral ischemia/reperfusion injury (CIRI) via Nrf2 pathway activation. Nrf2 activator-21 improves neurological function, alleviates anxiety-like behavior, enhances memory in rats with 2-vessel occlusion (2VO)-induced CIRI. Nrf2 activator-21 can be used for the study of cerebral ischemia/reperfusion injury .
    Nrf2 activator-21
  • HY-N1983R
    Caudatin (Standard)

    		Reference Standards Apoptosis Autophagy Reactive Oxygen Species (ROS) Mitochondrial Metabolism PARP Caspase Bcl-2 Family VEGFR FAK WDR5 p38 MAPK JNK PPAR Neurological Disease Inflammation/Immunology Cancer
    Caudatin (Standard) is the analytical standard of Caudatin (HY-N1983). This product is intended for research and analytical applications. Caudatin is an orally active and brain-penetrant C-21 steroidal found in Cynanchum bungei decne with a variety of biological activities. Caudatin can inhibit cell proliferation, migration, invasion, cause cell phase arrest, induce apoptosis, autophagy, ROS prodution and loss of mitochondrial membrane potential. Caudatin activates PARP, caspase-3, -7, -9, upregulates pro-apoptotic Bad and Bax and downregulates anti-apoptotic Bcl-2 and Bcl-XL. Caudatin suppresses VEGF, FAK phosphorylation, upregulates p21, p27, DR5 protein expression, activates the p38 MAPK, JNK and PPARα/TFEB-mediated autophagy-lysosomal signaling pathways. Caudatin can be used for the research of cancer, inflammation and neurological disease, such as glioma and Alzheimer's disease .
    Caudatin (Standard)
  • 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-143235
    BRD4 Inhibitor-15

    		Epigenetic Reader Domain Apoptosis Bcl-2 Family Caspase c-Myc Cancer
    BRD4 Inhibitor-15 (compound 13) is a potent BRD4 inhibitor, with an IC50 of 18 nM. BRD4 Inhibitor-15 induces apoptosis of 22RV1 cells by regulating Bcl-2/Bax proteins and activating caspase-3 signaling pathway. BRD4 Inhibitor-15 down-regulates the c-Myc level in 22RV1 cells. BRD4 Inhibitor-15 can be used for prostate cancer research .
    BRD4 Inhibitor-15

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