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Results for "

apoptotic inducible factor

" in MedChemExpress (MCE) Product Catalog:

30

Inhibitors & Agonists

1

Peptides

1

Inhibitory Antibodies

17

Natural
Products

Cat. No. Product Name Target Research Areas Chemical Structure
  • HY-N0784
    Ginkgolide B
    10+ Cited Publications

    BN-52021

    Platelet-activating Factor Receptor (PAFR) Apoptosis Cardiovascular Disease Neurological Disease Inflammation/Immunology Cancer
    Ginkgolide B (BN-52021), a terpene lactone, is a potent platelet activating factor antagonist. Ginkgolide B protects endothelial cells via the activation of PXR from injuries induced by xeno- and endobiotics. Ginkgolide B can pass through the brain-blood barrier. Ginkgolide B has anti-oxidant, anti-inflammatory, anti-tumor, and anti-apoptotic activity. Ginkgolide B has marked neuroprotective effects against ischemia-induced impairments .
    Ginkgolide B
  • HY-108635
    C16-PAF
    Maximum Cited Publications
    40 Publications Verification

    PAF (C16)

    p38 MAPK MEK ERK Endogenous Metabolite Cardiovascular Disease Inflammation/Immunology
    C16-PAF (PAF (C16)), a phospholipid mediator, is a platelet-activating factor and ligand for PAF G-protein-coupled receptor (PAFR). C16-PAF exhibits anti-apoptotic effect and inhibits caspase-dependent death by activating the PAFR. C16-PAF is a potent MAPK and MEK/ERK activator. C16-PAF induces increased vascular permeability .
    C16-PAF
  • HY-N6871
    Abietic acid
    3 Publications Verification

    Bacterial IKK Ferroptosis Infection Metabolic Disease Inflammation/Immunology Cancer
    Abietic acid, an orally active diterpene isolated from Colophony, displays significant anti-proliferative, anti-inflammatory, anti-obesity effect, bacteriostatic, cell cycle arresting and pro-apoptotic activities. Abietic acid inhibits lipoxygenase activity for allergy. Abietic acid enhances cell migration and tube formation in HUVECs. Abietic acid induces significant angiogenic potential, which is associated with upregulation of extracellular signal-regulated kinase (ERK) and p38 expression. Abietic acid attenuates sepsis-induced lung injury by inhibiting nuclear factor kappa-light-chain-enhancer of activated B cells (NF-κB) pathway to inhibit M1 macrophage polarization. Abietic acid exhibits a positive effect against liver injury by attenuating inflammation and ferroptosis. Abietic acid shows accelerated wound closure in a mouse model of cutaneous wounds. Abietic acid significantly reduces the proliferation and growth of NSCLC cells by IKKβ inhibition.Additionally, Abietic acid ameliorates psoriasis-like inflammation and modulates gut microbiota in mice. Abietic acid is promising for research in non-small-cell lung cancer (NSCLC), liver injury-related deseases and psoriasis .
    Abietic acid
  • HY-W040129
    Chromomycin A3
    1 Publications Verification

    DNA Alkylator/Crosslinker DNA/RNA Synthesis Apoptosis Caspase Infection Neurological Disease Cancer
    Chromomycin A3 is an inhibitor that selectively binds to GC-rich DNA sequences. Chromomycin A3 targets the DNA minor groove after forming a dimer with Mg 2+. Chromomycin A3 inhibits DNA replication and transcription, blocks the binding of Sp1 transcription factor to target gene promoters, downregulates the expression of anti-apoptotic proteins such as FLIP, Mcl-1, and XIAP, and induces S-phase cycle arrest and caspase-dependent apoptosis in tumor cells. Chromomycin A3 can antagonize oxidative stress induced by glutathione depletion and neuronal apoptosis induced by Camptothecin (HY-15660). Chromomycin A3 can be used in basic research on malignant tumors such as cholangiocarcinoma, and is a potential chemosensitizer and GC-rich region probe .
    Chromomycin A3
  • HY-N0103
    Sophocarpine
    10+ Cited Publications

    Autophagy Apoptosis NF-κB PI3K Akt MEK ERK PTEN Cardiovascular Disease Inflammation/Immunology Cancer
    Sophocarpine is a PTEN activator and an inhibitor of PI3K/Akt, MEK/ERK, and NF-κB signaling pathways. Sophocarpine upregulates PTEN expression and inhibits PI3K/Akt phosphorylation, arrests tumor cell cycle and induces apoptosis. Sophocarpine inhibits MEK/ERK phosphorylation and VEGF secretion, reducing tumor cell migration. Sophocarpine can also inhibit NF-κB activation and p38 and JNK phosphorylation, reduce the expression of inflammatory factors such as iNOS and COX-2, and activate the Nrf2/HO-1 pathway to reduce oxidative stress. Sophocarpine has anti-tumor, anti-inflammatory, antioxidant and anti-apoptotic effects, and can be used in the research of cancers such as glioblastoma and colorectal cancer, inflammation-related diseases, and Doxorubicin (HY-15142A)-induced cardiac damage .
    Sophocarpine
  • HY-10447

    EM-1421

    Survivin COX TNF Receptor Apoptosis Infection Inflammation/Immunology Cancer
    Terameprocol is an inhibitor targeting the Sp1 transcription factor, which can selectively inhibit the transcription of Sp1-dependent genes. Terameprocol exerts its effects by inhibiting Sp1-mediated gene transcription, such as reducing the expression of genes like CDC2, survivin and HMGB1, thereby arresting the cell cycle, inducing apoptosis, and suppressing the inflammatory response. Terameprocol exhibits anti-proliferative, pro-apoptotic, and anti-inflammatory activities and is currently mainly used in the research of diseases such as cancer and pulmonary arterial hypertension[1][2][3].
    Terameprocol
  • HY-N0863

    NSC-698790; Smilax saponin B

    Bcl-2 Family Apoptosis Akt c-Myc ERK p38 MAPK JNK FOXO Cancer
    Methyl protodioscin (NSC-698790; Smilax saponin B) is a multi-target, selective, steroidal diglycoside inhibitor with antitumor activity that induces cell cycle arrest. The mechanism of action of Methyl protodioscin is complex, involving the induction of G2/M cell cycle arrest, regulation of the Bcl-2/Bax apoptotic pathway, inhibition of the Akt1/c-Myc axis and MAPK/ERK signaling, while simultaneously downregulating ADAM15 and inducing FOXO1 to reduce cholesterol synthesis. It also inhibits the JNK/c-Jun pathway, reducing the production of inflammatory factors (IL-6, TNF-α). Methyl protodioscin exhibits significant antitumor (inhibiting proliferation, migration, invasion, and inducing apoptosis), anti-inflammatory, and anti-restenosis activities. Methyl protodioscin can be used in research on lung cancer, prostate cancer, pancreatic cancer, and other tumors, as well as inflammatory diseases such as airway inflammation and enteritis .
    Methyl protodioscin
  • HY-N6005

    Bacterial Fungal Apoptosis Bcl-2 Family Infection Metabolic Disease Cancer
    Methyl caffeate is a phenylpropanoid, antibacterial agent, and Apoptosis-inducing agent. Methyl caffeate can be isolated from the flowers of peach Prunus persica (L.). Methyl caffeate upregulates the expression of pro-apoptotic proteins Bid, Bax and p53, and downregulates the expression of anti-apoptotic protein BCL-2. Methyl caffeate downregulates SASP factors. Methyl caffeate enhances glucose-stimulated insulin secretion. Methyl caffeate inhibits the growth of Gram-positive bacteria, Gram-negative bacteria, fungi, and Mycobacterium tuberculosis strains. Methyl caffeate can be used in studies related to breast cancer, type 2 diabetes, and tuberculosis .
    Methyl caffeate
  • HY-W075770

    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-125305

    Caspase Apoptosis Cancer
    Z-AEVD-FMK is a caspase-10 inhibitor. Z-AEVD-FMK can inhibit the activation of Bid and the release of apoptosis-inducing factor (AIF) in mitochondria in cells, resulting in a significant decrease in the number of apoptotic cells .
    Z-AEVD-FMK
  • HY-158783

    Ceramidase Bcl-2 Family LPL Receptor Apoptosis Neurological Disease
    SACLAC, a Ceramide analog, is a potent and covalent acid ceramidase (ASAH1; AC) inhibitor with a Ki of 97.1 nM. SACLAC effectively blocks AC activity and induces a decrease in sphingosine 1-phosphate (S1P) and total ceramide levels. SACLAC reduces the levels of splicing factor SF3B1 and alternative Mcl-1 mRNA splicing, increases pro-apoptotic Mcl-1S levels to induce apoptosis in acute myeloid leukemia (AML) cells. SACLAC reduces the leukemic burden in human AML xenograft mouse models .
    SACLAC
  • HY-P3385

    SCB-313

    Drug Derivative Apoptosis Cancer
    Rilunermin alfa (SCB-313) is a recombinant fusion protein composed of the human C-propeptide of alpha1(I) collagen (Trimer-Tag) to the C-terminus of the mature human tumor necrosis factor (TNF)-related apoptosis-inducing ligand (TRAIL; Apo2L). Rilunermin alfa has potential pro-apoptotic and antineoplastic activities .
    Rilunermin alfa
  • HY-N0784R

    BN-52021 (Standard)

    Reference Standards Platelet-activating Factor Receptor (PAFR) Apoptosis Cardiovascular Disease Neurological Disease Inflammation/Immunology Cancer
    Ginkgolide B (Standard) is the analytical standard of Ginkgolide B. This product is intended for research and analytical applications. Ginkgolide B (BN-52021), a terpene lactone, is a potent platelet activating factor antagonist. Ginkgolide B protects endothelial cells via the activation of PXR from injuries induced by xeno- and endobiotics. Ginkgolide B can pass through the brain-blood barrier. Ginkgolide B has anti-oxidant, anti-inflammatory, anti-tumor, and anti-apoptotic activity. Ginkgolide B has marked neuroprotective effects against ischemia-induced impairments .
    Ginkgolide B (Standard)
  • HY-117359

    PAI-1 Apoptosis Cancer
    UCD38B hydrochloride is a cell permeant, competitive enzymatic uPA inhibitor with an IC50 value of 7 μM. UCD38B hydrochloride targets intracellular uPA causing mistrafficking of uPA into perinuclear mitochondria, reducing the mitochondrial membrane potential, and followed by the release of apoptotic inducible factor (AIF). UCD38B hydrochloride induces apoptosis .
    UCD38B hydrochloride
  • HY-N0103A
    Sophocarpine monohydrate
    10+ Cited Publications

    Autophagy Apoptosis NF-κB PI3K Akt MEK ERK Cardiovascular Disease Inflammation/Immunology Cancer
    Sophocarpine monohydrate is a PTEN activator and an inhibitor of PI3K/Akt, MEK/ERK, and NF-κB signaling pathways. Sophocarpine monohydrate upregulates PTEN expression and inhibits PI3K/Akt phosphorylation, arrests tumor cell cycle and induces apoptosis. Sophocarpine monohydrate inhibits MEK/ERK phosphorylation and VEGF secretion, reducing tumor cell migration. Sophocarpine monohydrate can also inhibit NF-κB activation and p38 and JNK phosphorylation, reduce the expression of inflammatory factors such as iNOS and COX-2, and activate the Nrf2/HO-1 pathway to reduce oxidative stress. Sophocarpine monohydrate has anti-tumor, anti-inflammatory, antioxidant and anti-apoptotic effects, and can be used in the research of cancers such as glioblastoma and colorectal cancer, inflammation-related diseases, and Doxorubicin (HY-15142A)-induced cardiac damage .
    Sophocarpine monohydrate
  • HY-157343A

    Apoptosis Mitochondrial Metabolism Caspase Neurological Disease Cancer
    GD3 Ganglioside sodium is an Apoptosis inducer and biomarker for mouse neural stem cells. GD3 Ganglioside sodium expresses in neural stem cells and the subventricular zone of the adult mouse brain. GD3 Ganglioside sodium targets the mitochondrial permeability transition pore complex, induces pore opening, dissipates mitochondrial transmembrane potential, triggers Mitochondrial swelling, releases pro-apoptotic factors, and activates Caspase-9. GD3 Ganglioside sodium is applicable to research related to glioblastoma .
    GD3 Ganglioside sodium
  • HY-157343

    Apoptosis Mitochondrial Metabolism Caspase Neurological Disease Cancer
    GD3 Ganglioside is an Apoptosis inducer and a biomarker for mouse neural stem cells. GD3 Ganglioside expresses in neural stem cells and the subventricular zone of the adult mouse brain. GD3 Ganglioside targets the mitochondrial permeability transition pore complex, induces pore opening, dissipates mitochondrial transmembrane potential, triggers Mitochondrial swelling, releases pro-apoptotic factors, and activates Caspase-9. GD3 Ganglioside is applicable to research related to glioblastoma .
    GD3 Ganglioside
  • HY-157343B

    Apoptosis Mitochondrial Metabolism Caspase Neurological Disease Cancer
    GD3 Ganglioside ammonium is an Apoptosis inducer and biomarker for mouse neural stem cells. GD3 Ganglioside ammonium expresses in neural stem cells and the subventricular zone of the adult mouse brain. GD3 Ganglioside ammonium targets the mitochondrial permeability transition pore complex, induces pore opening, dissipates mitochondrial transmembrane potential, triggers Mitochondrial swelling, releases pro-apoptotic factors, and activates Caspase-9. GD3 Ganglioside ammonium is applicable to research related to glioblastoma .
    GD3 Ganglioside ammonium
  • HY-N3204

    Apoptosis Neurological Disease
    Neoechinulin A is an isoprenyl indole alkaloid that exhibits scavenging, neurotrophic factor-like, and anti-apoptotic activities. Neoechinulin A induces memory improvements and antidepressant-like effects in mice .
    Neoechinulin A
  • HY-N10009

    NF-κB TNF Receptor COX ERK p38 MAPK Sirtuin Inflammation/Immunology
    Cudraflavone B is a prenylated flavonoid with anti-inflammatory and anti-tumor properties. Cudraflavone B is also a dual inhibitor of COX-1 and COX-2. Cudraflavone B blocks the translocation of nuclear factor κB (NF-κB) from the cytoplasm to the nucleus in macrophages. Thus, Cudraflavone B inhibits tumor necrosis factor α (TNFα) gene expression and secretion. Cudraflavone B also triggers the mitochondrial apoptotic pathway, activates NF-κB, the MAPK p38, and ERK, and induced the expression of SIRT1. Thus Cudraflavone B inhibits the growth of human oral squamous cell carcinoma cells .
    Cudraflavone B
  • HY-124665

    TNF Receptor Interleukin Related Infection Metabolic Disease Inflammation/Immunology
    LMP-420 is a selective tumor necrosis factor-α (TNF-α) inhibitor. LMP-420 reduces the release of pro-inflammatory cytokines (e.g., IL-1β, IL-2), inducing the expression of anti-inflammatory cytokine IL-10 and anti-apoptotic molecules SOCS-1 and Mn-SOD. LMP-420 also downregulates chemokines (e.g., IP-10, MCP-1) to reduce immune cell infiltration. LMP-420 is promising for research of type 1 diabetes mellitus, inflammatory diseases (e.g., colitis), and HIV-Mycobacterium tuberculosis coinfection .
    LMP-420
  • HY-171447

    Caspase Apoptosis Others
    LPT-99 is an antagonist of apoptotic protease activating factor 1 (APAF-1). LPT-99 suppresses the activation of procaspase-9. LPT99 suppresses Cisplatin (HY-17394)-induced apoptosis. LPT99 can effectively mitigate cisplatin-induced hearing loss in rats.
    LPT99
  • HY-N13123

    Apoptosis Cancer
    Tenacissoside C is an anti-cancer compound that inhibits angiogenesis. Tenacissoside C induces apoptosis in cancer cells by down-regulating the expression of anti-apoptotic factors and activating caspase-9 and caspase-3. Tenacissoside C also causes cell cycle arrest in cancer cells and induces apoptosis through the mitochondrial pathway.
    Tenacissoside C
  • HY-108635R

    PAF (C16) (Standard)

    p38 MAPK MEK ERK Endogenous Metabolite Reference Standards Cardiovascular Disease Inflammation/Immunology
    C16-PAF (Standard) is the analytical standard of C16-PAF. This product is intended for research and analytical applications. C16-PAF (PAF (C16)), a phospholipid mediator, is a platelet-activating factor and ligand for PAF G-protein-coupled receptor (PAFR). C16-PAF exhibits anti-apoptotic effect and inhibits caspase-dependent death by activating the PAFR. C16-PAF is a potent MAPK and MEK/ERK activator. C16-PAF induces increased vascular permeability .
    C16-PAF (Standard)
  • HY-W040129R

    Reference Standards Bacterial Fungal Apoptosis Antibiotic Infection Neurological Disease Cancer
    Chromomycin A3 (Standard) is the analytical standard of Chromomycin A3 (HY-W040129). This product is intended for research and analytical applications. Chromomycin A3 is an inhibitor that selectively binds to GC-rich DNA sequences. Chromomycin A3 targets the DNA minor groove after forming a dimer with Mg 2+. Chromomycin A3 inhibits DNA replication and transcription, blocks the binding of Sp1 transcription factor to target gene promoters, downregulates the expression of anti-apoptotic proteins such as FLIP, Mcl-1, and XIAP, and induces S-phase cycle arrest and caspase-dependent apoptosis in tumor cells. Chromomycin A3 can antagonize oxidative stress induced by glutathione depletion and neuronal apoptosis induced by Camptothecin (HY-15660). Chromomycin A3 can be used in basic research on malignant tumors such as cholangiocarcinoma, and is a potential chemosensitizer and GC-rich region probe .
    Chromomycin A3 (Standard)
  • HY-N0103R

    Reference Standards Autophagy Apoptosis NF-κB PI3K Akt MEK ERK Cardiovascular Disease Inflammation/Immunology Cancer
    Sophocarpine (Standard) is the analytical standard of Sophocarpine (HY-N0103). This product is intended for research and analytical applications. Sophocarpine is a PTEN activator and an inhibitor of PI3K/Akt, MEK/ERK, and NF-κB signaling pathways. Sophocarpine upregulates PTEN expression and inhibits PI3K/Akt phosphorylation, arrests tumor cell cycle and induces apoptosis. Sophocarpine inhibits MEK/ERK phosphorylation and VEGF secretion, reducing tumor cell migration. Sophocarpine can also inhibit NF-κB activation and p38 and JNK phosphorylation, reduce the expression of inflammatory factors such as iNOS and COX-2, and activate the Nrf2/HO-1 pathway to reduce oxidative stress. Sophocarpine has anti-tumor, anti-inflammatory, antioxidant and anti-apoptotic effects, and can be used in the research of cancers such as glioblastoma and colorectal cancer, inflammation-related diseases, and Doxorubicin (HY-15142A)-induced cardiac damage .
    Sophocarpine (Standard)
  • HY-111096

    Caspase Cardiovascular Disease Metabolic Disease
    IDN-7314 is a pan-Caspase inhibitor with an IC50 of 0.2-7 nM against all tested Caspases. IDN-7314 abrogates Jo2-induced caspase-3/7 activity. IDN-7314 reduces the procoagulant activity of tissue factor in hepatocytes. IDN-7314 is applicable to research related to chemically induced hepatitis, fulminant liver failure and apoptotic liver injury .
    IDN-7314
  • HY-N16771

    Caspase Apoptosis Bcl-2 Family Bacterial VEGFR Cancer
    Clausenidin is a selective inhibitor targeting apoptosis-related pathways, including the mitochondrial pathway and death receptor pathway, and vascular endothelial growth factor (VEGF). Clausenidin induces mitochondrial membrane depolarization by activating caspase-3, caspase-8 and caspase-9, upregulating the pro-apoptotic protein Bax and downregulating the anti-apoptotic protein Bcl-2. Clausenidin also inhibits VEGF expression and blocks angiogenesis, exerting anti-tumor activity. Clausenidin has inhibitory effects against Mycobacterium tuberculosis (MIC=200 μg/mL). Clausenidin can induce apoptosis in liver cancer cells, arrest the cell cycle in the G2/M phase, and inhibit tumor angiogenesis. Clausenidin can be used in the research of malignant tumors such as liver cancer .
    Clausenidin
  • HY-173365

    VEGFR Cancer
    VEGFR-2-IN-67 (Compound 6b) is an inhibitor of vascular endothelial growth factor receptor 2 (VEGFR-2). Its IC50 values for MDA-231 and MCF-7 cell lines are 5.91 µM and 7.16 µM respectively, and its inhibitory effect on VEGFR-2 is comparable to that of Sorafenib (HY-10201) (IC50 is 53.63 nM). VEGFR-2-IN-67 exerts significant anti-cancer activity through mechanisms such as inducing Apoptosis (the early apoptosis rate reaches 57.20%), arresting the cell cycle at the G1 phase, upregulating pro-apoptotic markers and downregulating Bcl-2. VEGFR-2-IN-67 can be used for research in the field of cancer .
    VEGFR-2-IN-67
  • HY-N14094

    JAK Apoptosis Autophagy Cancer
    Tubulosine is an alkaloid. Tubulosine can be isolated from Pogonopus tubulosus (DC.) Schumann. Tubulosine is an ATP-competitive, selective JAK3 inhibitor with an IC50 value of 9.9 nM. Tubulosine also inhibits the kinase activities of other JAK family members, the extent of inhibition is less than that of JAK3, with IC50 values of 69.5, 84.9 and 76.3 nM for JAK1, JAK2 and TYK2, respectively. Tubulosine selectively inhibits JAK3 signalling by binding to the ATP-binding site of the kinase of JAK3. Tubulosine induces apoptotic and necrotic/autophagic cell death. Tubulosine inhibits the process of peptide chain elongation by eukaryotic polysomes by, specifically preventing the elongation-factor-2-dependent step of translocation. Tubulosine exhibits anticancer activity in breast cancer cells .
    Tubulosine

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