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Results for "

apoptotic inducible factor

" in MedChemExpress (MCE) Product Catalog:

By Targets:	Akt (3) Antibiotic (1) Apoptosis (14) Autophagy (3) Bacterial (2) Bcl-2 Family (1) Caspase (2) Ceramidase (1) COX (2) DNA Alkylator/Crosslinker (1) DNA/RNA Synthesis (1) Endogenous Metabolite (2) ERK (6) Ferroptosis (1) Fungal (1) IKK (1) LPL Receptor (1) MEK (5) NF-κB (4) p38 MAPK (3) PAI-1 (1) PI3K (3) Platelet-activating Factor Receptor (PAFR) (2) PTEN (1) Reference Standards (3) Sirtuin (1) Survivin (1) TNF Receptor (2) VEGFR (1)
By Research Areas:	Cancer (13) Cardiovascular Disease (7) Infection (4) Inflammation/Immunology (10) Metabolic Disease (1) Neurological Disease (6)

By Targets:

Akt (3)

Antibiotic (1)

Apoptosis (14)

Autophagy (3)

Bacterial (2)

Bcl-2 Family (1)

Caspase (2)

Ceramidase (1)

COX (2)

DNA Alkylator/Crosslinker (1)

DNA/RNA Synthesis (1)

Endogenous Metabolite (2)

ERK (6)

Ferroptosis (1)

Fungal (1)

IKK (1)

LPL Receptor (1)

MEK (5)

NF-κB (4)

p38 MAPK (3)

PAI-1 (1)

PI3K (3)

Platelet-activating Factor Receptor (PAFR) (2)

PTEN (1)

Reference Standards (3)

Sirtuin (1)

Survivin (1)

TNF Receptor (2)

VEGFR (1)

By Research Areas:

Cancer (13)

Cardiovascular Disease (7)

Infection (4)

Inflammation/Immunology (10)

Metabolic Disease (1)

Neurological Disease (6)

Inhibitors & Agonists

Natural
Products

Targets Recommended: Salt-inducible Kinase (SIK) Itk HIF/HIF Prolyl-Hydroxylase AIM2

Cat. No.	Product Name	Target	Research Areas	Chemical Structure

HY-117359

UCD38B hydrochloride	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 .

HY-N3204

Neoechinulin A	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 .

HY-N0784

Ginkgolide B 5+ 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 .

HY-108635

C16-PAF Maximum Cited Publications 24 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 .

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 K_i 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 .

HY-171447

LPT99	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.

HY-N13123

Tenacissoside C	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.

HY-13559

Atiprimod Azaspirane	Apoptosis	Cancer
Atiprimod (Azaspirane) is an orally bioavailable small molecule with antitumor, anti-inflammatory, and anti-angiogenic activities. Atiprimod blocks the signaling pathways of interleukin-6 and vascular endothelial growth factor (VEGF) by inhibiting the phosphorylation of signal transducer and activator of transcription 3 (STAT3). Atiprimod also downregulates the anti-apoptotic proteins Bcl-2, Bcl-XL, and Mcl-1, thereby inhibiting cell proliferation, inducing cell cycle arrest, and inducing apoptosis. Atiprimod triggers persistent ER stress-mediated apoptosis in breast cancer cells by activating the PERK/eIF2α/ATF4/CHOP axis and inhibiting the nuclear translocation of STAT3/NF-κB transcription factors .

HY-N10009

Cudraflavone B	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 .

HY-N0784R

Ginkgolide B (Standard) 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 .

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 .

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].

HY-108635R

C16-PAF (Standard)	p38 MAPK MEK ERK Endogenous Metabolite	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 .

HY-W040129R

Chromomycin A3 (Standard)	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 .

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 .

HY-N0103A

Sophocarpine monohydrate 5+ 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 .

HY-N0103

Sophocarpine 5+ 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 .

HY-N0103R

Sophocarpine (Standard)	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 .

HY-N6871

Abietic acid	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 .

Cat. No.	Product Name	Category	Target	Chemical Structure