Search Result
Results for "
apoptotic cell membranes
" in MedChemExpress (MCE) Product Catalog:
1
Biochemical Assay Reagents
| Cat. No. |
Product Name |
Target |
Research Areas |
Chemical Structure |
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- HY-N9933
-
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TβMCA
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FXR
Apoptosis
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Neurological Disease
Metabolic Disease
Inflammation/Immunology
Cancer
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Tauro-β-muricholic acid (TβMCA) is an orally active trihydroxylated bile acid and a competitive, reversible FXR antagonist (IC50=40 μM). Tauro-β-muricholic acid inhibits bile acid-induced hepatocyte apoptosis by maintaining mitochondrial membrane potential, while simultaneously inhibiting intestinal FXR signaling, affecting bile acid synthesis, hepatic lipid metabolism, and insulin sensitivity. Accumulation of tauro-β-muricholic acid disrupts metabolic homeostasis, promoting cancer stem cell proliferation and tumor progression. The mechanisms of tauro-β-muricholic acid involve two aspects: first, inhibiting the translocation of the pro-apoptotic protein Bax to mitochondria and maintaining mitochondrial membrane potential (MMP); and second, blocking the FXR signaling pathway to regulate bile acid metabolism, reduce serum ceramide production, and downregulate the hepatic SREBP1C/CIDEA pathway. Tauro-β-muricholic acid possesses anti-hepatocyte apoptosis, bile acid homeostasis regulation, and liver fat accumulation reduction properties, and also functions as a biomarker, making it useful in the study of diseases such as bile acid metabolism disorders, non-alcoholic fatty liver disease, colorectal cancer, and liver fibrosis .
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- HY-A0183
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Phospholipids, phosphatidylserines; Serine glycerophosphatides
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Akt
TGF-β Receptor
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Inflammation/Immunology
|
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Phosphatidylserine (Phospholipids) is a well-conserved anti-inflammatory and immunosuppressive signal. Phosphatidylserine is involved in membrane translocation and the activation of protein kinase C, participating in Akt signaling through its interaction with PIP3. The local exposure of Phosphatidylserine can interact with complement and other proteins, promoting microglial phagocytosis during critical periods of synaptic refinement. Phosphatidylserine can promote blood coagulation in the extracellular environment and acts as a "eat me" signal to clear out apoptotic cells. Phosphatidylserine can suppress inflammation in tissues by inducing TGF-β secretion and inhibiting immune responses .
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- HY-137371
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Bacterial
Apoptosis
Antibiotic
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Infection
Cancer
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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].
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- HY-D0917
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DNA Stain
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Cancer
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NIR-Red Dead Cell-1 Dye is a DNA-binding fluorescent dye for non-living cells (Ex/Em=515 nm/531 nm). NIR-Red Dead Cell-1 Dye can intercalate into base pairs of double-stranded DNA and produce stronger fluorescence. NIR-Red Dead Cell-1 Dye is suitable for necrotic cells or late apoptotic cells with damaged cell membranes, showing green fluorescence under fluorescence microscopy or flow cytometry. NIR-Red Dead Cell-1 Dye can be used to distinguish live cells from dead cells and distinguish cell membrane integrity. NIR-Red Dead Cell-1 Dye can be attached to the surface of Feraheme (FH) nanoparticles (NPs) to obtain fluorescent dye-functionalized NPs for drug delivery studies .
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- HY-N1983
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Apoptosis
Autophagy
Reactive Oxygen Species (ROS)
Mitochondrial Metabolism
PARP
Caspase
Bcl-2 Family
VEGFR
FAK
WDR5
p38 MAPK
JNK
PPAR
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Neurological Disease
Inflammation/Immunology
Cancer
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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 .
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- HY-112624K
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Dextran 5; Dextran D5; Dextran T5(MW 4500-5500)
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Apoptosis
Autophagy
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Others
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Dextran T5 (MW 5,000) is a sulfated polysaccharide anti-apoptotic and autophagic agent. Dextran T5 (MW 5,000) has sulfated groups and interacts with cell membranes by mimicking endogenous glycosaminoglycans, inhibiting the mitochondrial apoptotic pathway and delaying DNA fragmentation to exert anti-apoptotic activity. Dextran T5 (MW 5,000) also promotes the conversion of LC3-I to LC3-II and the formation of autophagosomes to activate the autophagic pathway. Dextran T5 (MW 5,000) can prolong the survival cycle of CHO cells and increase the production of recombinant erythropoietin (EPO). The Dextran series of compounds are also natural polysaccharide drug carriers that can be connected to drugs through covalent bonding methods such as ester bonds, amide bonds or click chemistry, or self-assembled to form carriers such as nanoparticles and hydrogels. Dextran is biodegradable and biocompatible, and can achieve targeted delivery and controlled release of drugs. Dextran derivatives can prolong drug half-life, increase local concentration and reduce immune clearance activity. The Dextran series of compounds are also natural polysaccharide drug carriers that can be connected to drugs through covalent bonding methods such as ester bonds, amide bonds or click chemistry, or self-assembled to form carriers such as nanoparticles and hydrogels. Dextran is biodegradable and biocompatible, and can achieve targeted delivery and controlled release of drugs. Dextran derivatives can prolong the half-life of drugs, increase local concentrations, and reduce the activity of immune clearance .
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- HY-D0918
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Fluorescent Dye
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Others
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YO-PRO-1 is a non-cell-membrane-penetrating green fluorescent dye. YO-PRO-1 cannot penetrate normal cell membranes but can penetrate the membranes of apoptotic and necrotic cells. YO-PRO-1 has a high affinity for DNA. When it is not bound to DNA, it emits almost no fluorescence, and when it binds to DNA, it can emit green fluorescence (Ex/Em: 488/530±30 nM). YO-PRO-1 is often used together with Propidium Iodide (HY-D0815) to analyze and identify apoptotic and necrotic cells .
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- HY-P10943
-
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Fluorescent Dye
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Inflammation/Immunology
Cancer
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APO-15 is a phosphatidylserine-binding fluorescent probe and apoptosis imaging reagent. APO-15 exhibits high chemical stability under proteolytic and oxidative conditions, enables quantification and imaging of drug-induced apoptosis in preclinical mouse models, and is applicable to fixed tissue samples and multiple in vivo administration routes (Ex = 488 nm; Em = 525 nm). APO-15 can be used in studies related to acute lung injury and breast cancer .
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- HY-P1380A
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Apoptosis
Bcl-2 Family
Caspase
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Cancer
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Difopein TFA is a 14-3-3 protein inhibitor. Difopein TFA acts as an apoptosis inducer, regulates apoptosis-related proteins, downregulates Bcl-2, upregulates Bax, activates caspase-9 and caspase-3, and induces nuclear fragmentation, membrane-enclosed apoptotic bodies and DNA ladder formation. Difopein TFA serves as a tumor growth inhibitor, which inhibits the proliferation of glioma cells and induces their apoptosis in in vivo nude mouse models. Difopein TFA is applicable to glioma-related research .
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- HY-W017424
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Drug Intermediate
Caspase
Apoptosis
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Neurological Disease
Cancer
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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 .
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- HY-129746
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Apoptosis
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Cancer
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Arylquin 1, a prostate-apoptosis-response-4 (Par-4) secretagogue, targets vimentin to induce Par-4 secretion. Arylquin 1 induces non-apoptotic cell death in cancer cells through the induction of lysosomal membrane permeabilization (LMP) .
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- HY-N1989
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Na+/K+ ATPase
CaMK
Apoptosis
Cholinesterase (ChE)
NO Synthase
NF-κB
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Neurological Disease
Cancer
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Bacoside A is an orally active, blood-brain barrier-permeable triterpenoid saponin that modulates the activities of ATPases, AChE, CaMK2A and iNOS. Derived from Bacopa monniera. Bacoside A exerts significant antioxidant, anti-inflammatory and anti-apoptotic effects by maintaining ion balance, scavenging reactive oxygen species, stabilizing cell membranes, and regulating the expression of NF-κB and apoptosis-related proteins. Bacoside A counteracts morphine-induced reductions in Na +/K +-ATPase, Ca 2+-ATPase and Mg 2+-ATPase activities, increases mitochondrial membrane potential, and decreases intracellular reactive oxygen species levels. Bacoside A specifically binds to calcium/calmodulin-dependent protein kinase IIA to trigger endoplasmic reticulum calcium release. Bacoside A exhibits non-apoptotic cytotoxicity against glioblastoma cells while protecting normal nerve cells from stress-induced damage. Bacoside A is applicable to the research of Parkinson's disease and glioblastoma multiforme .
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- HY-W023144
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- HY-76573
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Apoptosis
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Cardiovascular Disease
Cancer
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ML-10 is a small molecule apoptosis probe. Due to the presence of fluorine atoms, ML-10 can be radiolabeled with 18F isotopes and can be used for apoptosis positron emission tomography imaging studies. ML-10 is selectively taken up and accumulated in apoptotic cells, while being excluded from live or necrotic cells. In addition, the uptake of ML-10 is associated with apoptotic features such as caspase activation, Annexin-V binding, and disruption of mitochondrial membrane potential .
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- HY-N6576
-
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p38 MAPK
ERK
JNK
IAP
PARP
Apoptosis
Caspase
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Cancer
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Hellebrigenin is an inhibitor that selectively targets the MAPK signaling pathway (ERK, p38, JNK) and XIAP, and can inhibit Akt expression and phosphorylation. Hellebrigenin can activate endogenous apoptosis pathways (such as mitochondrial membrane potential disruption, Caspase family activation, PARP cleavage), downregulate anti-apoptotic proteins (Bcl-2, Bcl-xL) and upregulate pro-apoptotic proteins (Bax, Bak). Hellebrigenin can also induce DNA double-strand breaks to activate the ATM pathway. Hellebrigenin can inhibit tumor cell proliferation and clone formation, and is mainly used in the study of oral squamous cell carcinoma, liver cancer and other cancers .
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- HY-117359
-
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PAI-1
Apoptosis
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Cancer
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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 .
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- HY-N1983R
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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 .
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- HY-178380
-
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HDAC
Reactive Oxygen Species (ROS)
Apoptosis
Necroptosis
Biochemical Assay Reagents
Caspase
Bcl-2 Family
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Inflammation/Immunology
Cancer
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HDAC8-IN-14, a curcuminoid derivative, is a selective HDAC8 inhibitor with a Ki of 9 nM. HDAC8-IN-14 induces the production of reactive oxygen species (ROS), disrupts mitochondrial membrane potential, and promotes apoptosis. HDAC8-IN-14 can significantly promote the accumulation of cells in the sub-G0/G1 phase, consistent with apoptotic or necrotic cell death. HDAC8-IN-14 induces upregulation of cytochrome c, cleaved caspase-3, and the pro-apoptotic protein Bak while leaving the anti-apoptotic Bcl-2 levels unaltered. HDAC8-IN-14 can be used for the study of leukemia .
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- HY-179155
-
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PI3K
mTOR
Apoptosis
Bcl-2 Family
MDM-2/p53
Telomerase
Mitochondrial Metabolism
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Inflammation/Immunology
Cancer
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PI3K/mTOR-IN-19 is an orally active, potent, selective PI3K (IC50 = 4.23 nM) and mTOR (IC50 = 2.3 nM) inhibitor. PI3K/mTOR-IN-19 significantly inhibits Eca109 cell viability and induces apoptosis. PI3K/mTOR-IN-19 causes G0/G1 cell cycle arrest, decreased mitochondrial membrane potential, and demonstrates marked telomerase inhibitory activity. PI3K/mTOR-IN-19 modulates the expression of key apoptotic regulators (Bcl-2, Bax, and p53) and downregulates the PI3K/Akt/mTOR signaling pathway. PI3K/mTOR-IN-19 can be used for the study of esophageal cancer .
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- HY-168720
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Apoptosis
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Cancer
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Apoptosis inducer 32 (Compound 7g) is an apoptosis inducer with a KD of 42 μM, showing anti-tumor activity. Apoptosis inducer 32 caused significant cellular morphological changes in MDA-MB-231 cells, including membrane bubbling, nuclear fragmentation, and apoptotic body formation. The IC50 of Apoptosis inducer 32 in MCF-7, MDA-MB-231, and HEK cells is 4.77, 6.56 and 337.8 μM respectively .
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- HY-167255
-
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Fluorescent Dye
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Others
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JC-10 is a lipophilic mitochondrial membrane potential indicator and is a fluorescent dye. JC-10 accumulates and aggregates in healthy mitochondria to emit red fluorescence; exists as a monomer emitting green fluorescence in the cytosol or apoptotic cells with collapsed mitochondrial membrane potential, enabling measurement of mitochondrial depolarization via the green/red fluorescence ratio .
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- HY-P10370B
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Apoptosis
Caspase
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Cancer
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d-(KLAKLAK)2, Proapoptotic Peptide acetate is a pro-Apoptotic peptide whose core mechanism of action is to disrupt organelle membranes, especially mitochondrial membranes, thereby inducing apoptosis. d-(KLAKLAK)2, Proapoptotic Peptide acetate activates the activity of caspase 3/7 in cancer cells. Although d-(KLAKLAK)2 Proapoptotic Peptide acetate exhibits very low toxicity to eukaryotic cells extracellularly, it cannot effectively penetrate cell membranes to enter the cytoplasm on its own. d-(KLAKLAK)2, Proapoptotic Peptide acetate must be conjugated with a carrier capable of "homing" and "internalization" to exert its anti-cancer effects .
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- HY-W800105
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Apoptosis
Reactive Oxygen Species (ROS)
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Cancer
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Geranyl isovalerate is a chemical component that can be extracted from Argyreia Nervosa. Geranyl isovalerate inhibits cancer cell proliferation in a dose-dependent and time-dependent manner. Geranyl isovalerate activates the apoptotic pathway by inducing mitochondrial membrane potential loss and ROS accumulation. Geranyl isovalerate can be used for cancer research .
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- HY-182586
-
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Fungal
Bcl-2 Family
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Infection
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Decyl gallate is an antifungal (fungal) agent. Decyl gallate downregulates the expression of the pro-apoptotic (apoptosis) protein Bak, upregulates the expression of the anti-apoptotic protein Bcl-2, and inhibits DNA damage. Decyl gallate disrupts ALG12-mediated N-glycosylation, overactivates the UPR pathway, and simultaneously reduces fungal cell wall enzyme activity, chitin levels, mitochondrial activity, budding ability, cell viability, and host cell adhesion capacity. Decyl gallate reduces inflammatory responses induced by fungal infection and disrupts fungal membrane structure. Decyl gallate can be used in studies related to paracoccidioidomycosis and invasive fungal infections .
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- HY-N16771
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Caspase
Apoptosis
Bcl-2 Family
Bacterial
VEGFR
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Cancer
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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 .
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- HY-P1380
-
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Apoptosis
Bcl-2 Family
Caspase
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Cancer
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Difopein is a 14-3-3 protein inhibitor. Difopein acts as an apoptosis inducer, regulates apoptosis-related proteins, downregulates Bcl-2, upregulates Bax, activates caspase-9 and caspase-3, and induces nuclear fragmentation, membrane-enclosed apoptotic bodies and DNA ladder formation. Difopein serves as a tumor growth inhibitor, which inhibits the proliferation of glioma cells and induces their apoptosis in in vivo nude mouse models. Difopein is applicable to glioma-related research .
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- HY-N17652
-
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Apoptosis
Mitochondrial Metabolism
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Cancer
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13′-Hydroxy-δ-tocopherol is a metabolite of long-chain vitamin E. 13′-Hydroxy-δ-tocopherol can induces cells apoptosis and minor reduction in mitochondrial membrane potential. 13′-Hydroxy-δ-tocopherol can be used for the research of hepatocellular carcinoma .
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- HY-183327
-
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PI3K
mTOR
Akt
Apoptosis
Reactive Oxygen Species (ROS)
Mitochondrial Metabolism
Bcl-2 Family
Caspase
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Cancer
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PI3K/mTOR-IN-22 is an orally active PI3K/mTOR kinase dual inhibitor with IC50 values of 400.5 nM and 8.2 nM. PI3K/mTOR-IN-22 downregulates phosphorylation of the AKT and mTOR, upregulates pro-apoptotic proteins Bax and caspase-3 and downregulates anti-apoptotic protein Bcl-2. PI3K/mTOR-IN-22 exhibits antiproliferative activity against cancer cells, induces apoptosis and ROS production, and reduces mitochondrial membrane potential. PI3K/mTOR-IN-22 exhibits antitumor activity in breast cancer mice models .
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- HY-183355
-
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Ras
ERK
Akt
Reactive Oxygen Species (ROS)
Apoptosis
Bcl-2 Family
Caspase
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Cancer
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KRAS G12D-IN-37 is a KRAS G12D inhibitor. KRAS G12D-IN-37 shows antiproliferative activity against KRAS G12D mutant tumor cells and minimal cytotoxicity toward normal cells. KRAS G12D-IN-37 binds stably to KRAS G12D via hydrogen bond interactions with residues His 95, Arg 68, and Asp 12, and inhibits downstream ERK/AKT signaling pathways. KRAS G12D-IN-37 elevates ROS levels, induces apoptosis, disrupts mitochondrial membrane potential. KRAS G12D-IN-37 downregulates the level of anti-apoptotic protein Bcl-2, and upregulates the levels of pro-apoptotic proteins Bax and caspase 3. KRAS G12D-IN-37 can be used for the research of cancer, such as gastric adenocarcinoma and colorectal cancer .
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- HY-W715812
-
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Fungal
Apoptosis
Caspase
Reactive Oxygen Species (ROS)
MDM-2/p53
SOD
Bcl-2 Family
PERK
JNK
p38 MAPK
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Cardiovascular Disease
Infection
Endocrinology
Cancer
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Bromuconazole is a triazole fungicide with oral efficacy and blood-brain barrier permeability . Bromuconazole protects crops from various fungal contaminations. Bromuconazole exhibits cytotoxicity against a variety of cancer cells, induces G0/G1 cell cycle arrest and inhibits DNA synthesis in cancer cells, and triggers cytoskeletal structural disorder, genotoxic damage, apoptotic (apoptosis) cell death, and mitochondrial membrane depolarization. Bromuconazole activates caspase-3, induces excessive production of ROS, p53 and Bax, lipid peroxidation, increased activities of SOD and CAT, and downregulates Bcl-2. By upregulating p-ERK1/2 and p-JNK, Bromuconazole disrupts the MAPK signaling pathway, impairs the cellular stress response of human trophoblast cells and endometrial cells, and damages the implantation process . Bromuconazole is applicable to research related to glioma, colon cancer, reproductive injury (implantation dysfunction), and cardiac dysfunction .
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- HY-181746
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Bcl-2 Family
Apoptosis
Caspase
PARP
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Cancer
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Bcl-2/Mcl-1-IN-5 (Compound S6) is a Bcl-2 and Mcl-1 inhibitor. Bcl-2/Mcl-1-IN-5 promotes Apoptosis, downregulates anti-apoptotic proteins Bcl-2 and Mcl-1, induces mitochondrial membrane potential depolarization, and activates the Caspase-dependent apoptotic cascade, as evidenced by Caspase-3 activation and PARP1 cleavage. Bcl-2/Mcl-1-IN-5 has anti-hepatocellular carcinoma activity .
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HY-L168
-
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643 compounds
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Extracellular vesicles (EVs) are small membrane binding structures that are released from cells into the surrounding environment and play a crucial role in mediating and regulating intercellular communication related to physiological and pathological processes. EVs are lipid membrane vesicles composed of proteins, lipids, and nucleic acids. EVs can be divided into several types based on their source, such as extracellular vesicles, microcapsules, and apoptotic vesicles. The size range of exosomes is 30-150nm, which are endocrine in multi vesicular endosomes (MVEs); microvesicles (50-1000nm) are secreted directly through extracellular interactions, thereby releasing plasma membrane vesicles. In contrast, apoptotic bodies are usually larger, ranging in size from 1 to 5 μ m. This is generated during programmed cell death. EV plays a crucial role in transmitting information between cells and influencing the behavior and function of receptor cells.
MCE designs a unique collection of 643 small molecules related to extracellular vesicles (EVs). It is a good tool to be used for research on metabolize, cancer and other diseases.
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HY-L144
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1,014 compounds
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Normal mitochondrial function is critical for maintaining cellular homeostasis because mitochondria produce ATP and are the major intracellular source of free radicals. Cellular dysfunctions induced by intracellular or extracellular insults converge on mitochondria and induce a sudden increase in permeability on the inner mitochondrial membrane, the so-called mitochondrial membrane permeability transition (MMPT). MMPT is caused by the opening of pores in the inner mitochondrial membrane, matrix swelling, and outer membrane rupture. The MMPT is an endpoint to initiate cell death because the pore opening together with the release of mitochondrial cytochrome c activates the apoptotic pathway of caspases.
The normal operation of mitochondrial function is important for maintaining normal cell death and treatment of mitochondrial diseases. MCE offers a unique collection of 1,014 compounds with identified and potential mitochondrial protective activity. MCE Mitochondrial Protection Compound Library is critical for drug discovery and development.
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| Cat. No. |
Product Name |
Type |
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- HY-D0917
-
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Fluorescent Dyes
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NIR-Red Dead Cell-1 Dye is a DNA-binding fluorescent dye for non-living cells (Ex/Em=515 nm/531 nm). NIR-Red Dead Cell-1 Dye can intercalate into base pairs of double-stranded DNA and produce stronger fluorescence. NIR-Red Dead Cell-1 Dye is suitable for necrotic cells or late apoptotic cells with damaged cell membranes, showing green fluorescence under fluorescence microscopy or flow cytometry. NIR-Red Dead Cell-1 Dye can be used to distinguish live cells from dead cells and distinguish cell membrane integrity. NIR-Red Dead Cell-1 Dye can be attached to the surface of Feraheme (FH) nanoparticles (NPs) to obtain fluorescent dye-functionalized NPs for drug delivery studies .
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- HY-D0918
-
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Fluorescent Dyes
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YO-PRO-1 is a non-cell-membrane-penetrating green fluorescent dye. YO-PRO-1 cannot penetrate normal cell membranes but can penetrate the membranes of apoptotic and necrotic cells. YO-PRO-1 has a high affinity for DNA. When it is not bound to DNA, it emits almost no fluorescence, and when it binds to DNA, it can emit green fluorescence (Ex/Em: 488/530±30 nM). YO-PRO-1 is often used together with Propidium Iodide (HY-D0815) to analyze and identify apoptotic and necrotic cells .
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- HY-167255
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Fluorescent Dyes
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JC-10 is a lipophilic mitochondrial membrane potential indicator and is a fluorescent dye. JC-10 accumulates and aggregates in healthy mitochondria to emit red fluorescence; exists as a monomer emitting green fluorescence in the cytosol or apoptotic cells with collapsed mitochondrial membrane potential, enabling measurement of mitochondrial depolarization via the green/red fluorescence ratio .
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| Cat. No. |
Product Name |
Type |
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- HY-112624K
-
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Dextran 5; Dextran D5; Dextran T5(MW 4500-5500)
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Biochemical Assay Reagents
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Dextran T5 (MW 5,000) is a sulfated polysaccharide anti-apoptotic and autophagic agent. Dextran T5 (MW 5,000) has sulfated groups and interacts with cell membranes by mimicking endogenous glycosaminoglycans, inhibiting the mitochondrial apoptotic pathway and delaying DNA fragmentation to exert anti-apoptotic activity. Dextran T5 (MW 5,000) also promotes the conversion of LC3-I to LC3-II and the formation of autophagosomes to activate the autophagic pathway. Dextran T5 (MW 5,000) can prolong the survival cycle of CHO cells and increase the production of recombinant erythropoietin (EPO). The Dextran series of compounds are also natural polysaccharide drug carriers that can be connected to drugs through covalent bonding methods such as ester bonds, amide bonds or click chemistry, or self-assembled to form carriers such as nanoparticles and hydrogels. Dextran is biodegradable and biocompatible, and can achieve targeted delivery and controlled release of drugs. Dextran derivatives can prolong drug half-life, increase local concentration and reduce immune clearance activity. The Dextran series of compounds are also natural polysaccharide drug carriers that can be connected to drugs through covalent bonding methods such as ester bonds, amide bonds or click chemistry, or self-assembled to form carriers such as nanoparticles and hydrogels. Dextran is biodegradable and biocompatible, and can achieve targeted delivery and controlled release of drugs. Dextran derivatives can prolong the half-life of drugs, increase local concentrations, and reduce the activity of immune clearance .
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| Cat. No. |
Product Name |
Target |
Research Area |
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- HY-P10943
-
|
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Fluorescent Dye
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Inflammation/Immunology
Cancer
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APO-15 is a phosphatidylserine-binding fluorescent probe and apoptosis imaging reagent. APO-15 exhibits high chemical stability under proteolytic and oxidative conditions, enables quantification and imaging of drug-induced apoptosis in preclinical mouse models, and is applicable to fixed tissue samples and multiple in vivo administration routes (Ex = 488 nm; Em = 525 nm). APO-15 can be used in studies related to acute lung injury and breast cancer .
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- HY-P1380A
-
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Apoptosis
Bcl-2 Family
Caspase
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Cancer
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Difopein TFA is a 14-3-3 protein inhibitor. Difopein TFA acts as an apoptosis inducer, regulates apoptosis-related proteins, downregulates Bcl-2, upregulates Bax, activates caspase-9 and caspase-3, and induces nuclear fragmentation, membrane-enclosed apoptotic bodies and DNA ladder formation. Difopein TFA serves as a tumor growth inhibitor, which inhibits the proliferation of glioma cells and induces their apoptosis in in vivo nude mouse models. Difopein TFA is applicable to glioma-related research .
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- HY-P10370B
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Apoptosis
Caspase
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Cancer
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d-(KLAKLAK)2, Proapoptotic Peptide acetate is a pro-Apoptotic peptide whose core mechanism of action is to disrupt organelle membranes, especially mitochondrial membranes, thereby inducing apoptosis. d-(KLAKLAK)2, Proapoptotic Peptide acetate activates the activity of caspase 3/7 in cancer cells. Although d-(KLAKLAK)2 Proapoptotic Peptide acetate exhibits very low toxicity to eukaryotic cells extracellularly, it cannot effectively penetrate cell membranes to enter the cytoplasm on its own. d-(KLAKLAK)2, Proapoptotic Peptide acetate must be conjugated with a carrier capable of "homing" and "internalization" to exert its anti-cancer effects .
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- HY-P1380
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Apoptosis
Bcl-2 Family
Caspase
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Cancer
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Difopein is a 14-3-3 protein inhibitor. Difopein acts as an apoptosis inducer, regulates apoptosis-related proteins, downregulates Bcl-2, upregulates Bax, activates caspase-9 and caspase-3, and induces nuclear fragmentation, membrane-enclosed apoptotic bodies and DNA ladder formation. Difopein serves as a tumor growth inhibitor, which inhibits the proliferation of glioma cells and induces their apoptosis in in vivo nude mouse models. Difopein is applicable to glioma-related research .
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| Cat. No. |
Product Name |
Category |
Target |
Chemical Structure |
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- HY-N9933
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TβMCA
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Structural Classification
Human Gut Microbiota Metabolites
Animals
Endogenous metabolite
Steroids
Source Classification
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FXR
Apoptosis
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Tauro-β-muricholic acid (TβMCA) is an orally active trihydroxylated bile acid and a competitive, reversible FXR antagonist (IC50=40 μM). Tauro-β-muricholic acid inhibits bile acid-induced hepatocyte apoptosis by maintaining mitochondrial membrane potential, while simultaneously inhibiting intestinal FXR signaling, affecting bile acid synthesis, hepatic lipid metabolism, and insulin sensitivity. Accumulation of tauro-β-muricholic acid disrupts metabolic homeostasis, promoting cancer stem cell proliferation and tumor progression. The mechanisms of tauro-β-muricholic acid involve two aspects: first, inhibiting the translocation of the pro-apoptotic protein Bax to mitochondria and maintaining mitochondrial membrane potential (MMP); and second, blocking the FXR signaling pathway to regulate bile acid metabolism, reduce serum ceramide production, and downregulate the hepatic SREBP1C/CIDEA pathway. Tauro-β-muricholic acid possesses anti-hepatocyte apoptosis, bile acid homeostasis regulation, and liver fat accumulation reduction properties, and also functions as a biomarker, making it useful in the study of diseases such as bile acid metabolism disorders, non-alcoholic fatty liver disease, colorectal cancer, and liver fibrosis .
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- HY-A0183
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Phospholipids, phosphatidylserines; Serine glycerophosphatides
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Animals
Source Classification
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Akt
TGF-β Receptor
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Phosphatidylserine (Phospholipids) is a well-conserved anti-inflammatory and immunosuppressive signal. Phosphatidylserine is involved in membrane translocation and the activation of protein kinase C, participating in Akt signaling through its interaction with PIP3. The local exposure of Phosphatidylserine can interact with complement and other proteins, promoting microglial phagocytosis during critical periods of synaptic refinement. Phosphatidylserine can promote blood coagulation in the extracellular environment and acts as a "eat me" signal to clear out apoptotic cells. Phosphatidylserine can suppress inflammation in tissues by inducing TGF-β secretion and inhibiting immune responses .
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-
- HY-N1983
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Structural Classification
Classification of Application Fields
Asclepiadaceae
Cynanchum otophyllum Schneid.
Cynanchum auriculatum Royle ex Wight
Plants
Disease Research Fields
Steroids
Source Classification
Cancer
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Apoptosis
Autophagy
Reactive Oxygen Species (ROS)
Mitochondrial Metabolism
PARP
Caspase
Bcl-2 Family
VEGFR
FAK
WDR5
p38 MAPK
JNK
PPAR
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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 .
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- HY-N1989
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Triterpenes
Structural Classification
Classification of Application Fields
Terpenoids
Scrophulariaceae
Metabolic Disease
Plants
Disease Research Fields
Bacopa monnieri (Linn.) Wettst.
Source Classification
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Na+/K+ ATPase
CaMK
Apoptosis
Cholinesterase (ChE)
NO Synthase
NF-κB
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Bacoside A is an orally active, blood-brain barrier-permeable triterpenoid saponin that modulates the activities of ATPases, AChE, CaMK2A and iNOS. Derived from Bacopa monniera. Bacoside A exerts significant antioxidant, anti-inflammatory and anti-apoptotic effects by maintaining ion balance, scavenging reactive oxygen species, stabilizing cell membranes, and regulating the expression of NF-κB and apoptosis-related proteins. Bacoside A counteracts morphine-induced reductions in Na +/K +-ATPase, Ca 2+-ATPase and Mg 2+-ATPase activities, increases mitochondrial membrane potential, and decreases intracellular reactive oxygen species levels. Bacoside A specifically binds to calcium/calmodulin-dependent protein kinase IIA to trigger endoplasmic reticulum calcium release. Bacoside A exhibits non-apoptotic cytotoxicity against glioblastoma cells while protecting normal nerve cells from stress-induced damage. Bacoside A is applicable to the research of Parkinson's disease and glioblastoma multiforme .
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- HY-N6576
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|
|
Animals
Classification of Application Fields
Disease Research Fields
Steroids
Source Classification
Cancer
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p38 MAPK
ERK
JNK
IAP
PARP
Apoptosis
Caspase
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Hellebrigenin is an inhibitor that selectively targets the MAPK signaling pathway (ERK, p38, JNK) and XIAP, and can inhibit Akt expression and phosphorylation. Hellebrigenin can activate endogenous apoptosis pathways (such as mitochondrial membrane potential disruption, Caspase family activation, PARP cleavage), downregulate anti-apoptotic proteins (Bcl-2, Bcl-xL) and upregulate pro-apoptotic proteins (Bax, Bak). Hellebrigenin can also induce DNA double-strand breaks to activate the ATM pathway. Hellebrigenin can inhibit tumor cell proliferation and clone formation, and is mainly used in the study of oral squamous cell carcinoma, liver cancer and other cancers .
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-
- HY-N1983R
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|
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Structural Classification
Asclepiadaceae
Cynanchum otophyllum Schneid.
Cynanchum auriculatum Royle ex Wight
Plants
Steroids
Source Classification
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Reference Standards
Apoptosis
Autophagy
Reactive Oxygen Species (ROS)
Mitochondrial Metabolism
PARP
Caspase
Bcl-2 Family
VEGFR
FAK
WDR5
p38 MAPK
JNK
PPAR
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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 .
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- HY-W800105
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- HY-N16771
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Structural Classification
Rutaceae
Coumarins
Phenylpropanoids
Plants
Clausena excavata N. L. Burman
Source Classification
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Caspase
Apoptosis
Bcl-2 Family
Bacterial
VEGFR
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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 .
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- HY-N17652
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