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Results for "

proapoptotic factor

" in MedChemExpress (MCE) Product Catalog:

20

Inhibitors & Agonists

1

Biochemical Assay Reagents

1

Peptides

1

Inhibitory Antibodies

5

Natural
Products

1

Isotope-Labeled Compounds

Cat. No. Product Name Target Research Areas Chemical Structure
  • 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-10496
    SC75741
    Maximum Cited Publications
    32 Publications Verification

    		 NF-κB Influenza Virus Infection Cancer
    SC75741 is a broad and efficient NF-κB inhibitor with an IC50 of 200 nM for p65 . SC75741 blocks influenza viruses (IV) replication. SC75741 impairs DNA binding of the NF-κB subunit p65, resulting in reduced expression of cytokines, chemokines, and pro-apoptotic factors. SC75741 subsequently inhibits caspase activation and blocks caspase-mediated nuclear export of viral ribonucleoproteins .
    SC75741
  • HY-N0060B
    (E)-Ferulic acid
    1 Publications Verification

    (E)-Coniferic acid

    		 β-catenin Bcl-2 Family Ferroptosis Endogenous Metabolite Cancer
    (E)-Ferulic acid is an isomer of ferulic acid, an aromatic compound abundant in plant cell walls. (E)-Ferulic acid causes phosphorylation of β-catenin (β-catenin), leading to proteasome degradation, increasing the expression of pro-apoptotic factor Bax and reducing pro-apoptotic factor Expression of the survival factor survivin. (E)-Ferulic acid can effectively remove reactive oxygen species (ROS) and inhibit lipid peroxidation. (E)-Ferulic acid exerts antiproliferative and antimigratory effects in the human lung cancer cell line H1299.
    (E)-Ferulic acid
  • HY-10447
    Terameprocol

    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-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-N6005
    Methyl caffeate

    		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-N0060BS
    (E)-Ferulic acid-d3

    (E)-Coniferic acid-d3

    		 β-catenin Bcl-2 Family Ferroptosis Endogenous Metabolite Cancer
    (E)-Ferulic acid-d3 is the deuterium labeled (E)-Ferulic acid. (E)-Ferulic acid is a isomer of Ferulic acid which is an aromatic compound, abundant in plant cell walls. (E)-Ferulic acid causes the phosphorylation of β-catenin, resulting in proteasomal degradation of β-catenin and increases the expression of pro-apoptotic factor Bax and decreases the expression of pro-survival factor survivin. (E)-Ferulic acid shows a potent ability to remove reactive oxygen species (ROS) and inhibits lipid peroxidation. (E)-Ferulic acid exerts both anti-proliferation and anti-migration effects in the human lung cancer cell line H1299 .
    (E)-Ferulic acid-d3
  • HY-158783
    SACLAC

    		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
    Rilunermin alfa

    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-157343A
    GD3 Ganglioside sodium

    		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
    GD3 Ganglioside

    		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
    GD3 Ganglioside ammonium

    		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-W145695
    Chitoheptaose

    		Biochemical Assay Reagents Apoptosis Interleukin Related IFNAR Cardiovascular Disease Inflammation/Immunology
    Chitoheptaose is an orally active chitooligosaccharide (degree of polymerization = 7). Chitoheptaose can be extracted from the exoskeletons of crustaceans, such as the shells of crabs, shrimps and lobsters. Chitoheptaose reduces pro-inflammatory cytokines while increasing the levels of anti-inflammatory cytokines (decreasing the levels of pro-inflammatory cytokines IL-1β, IL-17A and IFN-γ, and increasing the level of the anti-inflammatory cytokine IL-10). Chitoheptaose possesses antioxidant, anti-inflammatory and anti-Apoptotic activities. Chitoheptaose improves cardiac parameters, alleviates myocarditis injury, and exerts cardioprotective effects in a rat model of myocarditis. Chitoheptaose can be used in studies related to myocarditis .
    Chitoheptaose
  • HY-N0060BR
    (E)-Ferulic acid (Standard)

    (E)-Coniferic acid (Standard)

    		 Reference Standards β-catenin Bcl-2 Family Ferroptosis Endogenous Metabolite Cancer
    (E)-Ferulic acid (Standard) is the analytical standard of (E)-Ferulic acid. This product is intended for research and analytical applications. (E)-Ferulic acid is an isomer of ferulic acid, an aromatic compound abundant in plant cell walls. (E)-Ferulic acid causes phosphorylation of β-catenin (β-catenin), leading to proteasome degradation, increasing the expression of pro-apoptotic factor Bax and reducing pro-apoptotic factor Expression of the survival factor survivin. (E)-Ferulic acid can effectively remove reactive oxygen species (ROS) and inhibit lipid peroxidation. (E)-Ferulic acid exerts antiproliferative and antimigratory effects in the human lung cancer cell line H1299.
    (E)-Ferulic acid (Standard)
  • HY-141876
    PRT543

    		Histone Methyltransferase Notch PI3K Akt Bcl-2 Family DNA/RNA Synthesis Cancer
    PRT543 is an orally active selective PRMT5 inhibitor. PRT543 reduces intracellular symmetric dimethylarginine (sDMA) levels, downregulates the expression of genes related to DNA damage repair and DNA replication pathways, and induces abnormal alternative splicing. PRT543 inhibits the MYB, NOTCH1 and PI3K/AKT signaling pathways, promotes nuclear translocation of FOXO1, upregulates the pro-apoptotic protein BAX, and enhances cellular sensitivity to BCL-2 inhibition. PRT543 disrupts the normal RNA splicing process and exerts a synthetic lethal effect on myeloid tumor cells carrying splicing factor mutations. PRT543 can be used in research related to various cancers including breast cancer, ovarian cancer and acute myeloid leukemia .
    PRT543
  • HY-16366A
    Briciclib sodium

    ON 014185 sodium

    		 Eukaryotic Initiation Factor (eIF) CDK c-Myc MDM-2/p53 Caspase Apoptosis Cancer
    Briciclib (ON 014185) sodium is a eukaryotic translation initiation factor 4E (eIF4E) inhibitor. Briciclib sodium exhibits broad-spectrum anti-cancer activity, including in mantle cell leukemia, breast cancer, gastric cancer, and esophageal cancer cells. Briciclib sodium reduces the expression of cyclin D1 and c-Myc, and enhances the expression of P53 and Cleaved Caspase 3 pro-apoptotic proteins. Briciclib sodium can be used for the study of hematological system tumors and solid tumors .
    Briciclib sodium
  • HY-180157
    CDK2-IN-51

    		CDK Cancer
    CDK2-IN-51 is a pyrazolopyridine derivative, a CDK2 inhibitor with an IC50 of 23.47 nM. CDK2-IN-51 does not have a pro-apoptotic effect and had no significant effect on CDK2 protein expression. CDK2-IN-51 reduces expression of DNA replication factors (Polα, MCM7, ORC2, and ORC4) and pre-G1 cell cycle arrest. CDK2-IN-51 can be used for the research of colorectal cancer .
    CDK2-IN-51
  • HY-10496R
    SC75741 (Standard)

    		Reference Standards NF-κB Influenza Virus Infection Cancer
    SC75741 (Standard) is the analytical standard of SC75741 (HY-10496). This product is intended for research and analytical applications. SC75741 is a broad and efficient NF-κB inhibitor with an IC50 of 200 nM for p65 . SC75741 blocks influenza viruses (IV) replication. SC75741 impairs DNA binding of the NF-κB subunit p65, resulting in reduced expression of cytokines, chemokines, and pro-apoptotic factors. SC75741 subsequently inhibits caspase activation and blocks caspase-mediated nuclear export of viral ribonucleoproteins .
    SC75741 (Standard)
  • HY-173365
    VEGFR-2-IN-67

    		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-N16771
    Clausenidin

    		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

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