Cerebrovascular disease refers to a group of conditions that affect the blood vessels supplying the brain, leading to impaired blood flow and potential damage to brain tissue. This includes ischemic stroke, caused by blockage of blood vessels, and hemorrhagic stroke, resulting from bleeding in or around the brain. These conditions are major components of cardiovascular diseases (CVDs), which also encompass hypertension, heart attack, and other disorders related to the heart and circulatory system. Cerebrovascular diseases are significant causes of disability and mortality worldwide, often linked to shared risk factors such as high blood pressure, diabetes, smoking, obesity, and atherosclerosis. Early detection, management of risk factors, and prompt treatment are crucial in reducing the incidence and severity of these conditions.
Cerebrovascular Disease (113):
| Cat. No. |
Product Name |
CAS No. |
Purity |
Chemical Structure |
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- HY-112879
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Mito-TEMPO
|
1334850-99-5 |
99.19% |
|
Mito-TEMPO is a mitochondria-targeted antioxidant. Mito-TEMPO induces mitophagy by activating the PINK1/Parkin pathway, inhibits NLRP3 inflammasome activation, restores mitochondrial membrane potential, and improves renal function and podocyte injury. Mito-TEMPO regulates Ca2+ homeostasis, inhibits Bnip3 overexpression, shortens action potential duration, and exerts antiarrhythmic effects. Mito-TEMPO reverses premature senescence, reduces trabecular bone loss, and decreases cell apoptosis. Mito-TEMPO can be used in studies of chronic kidney disease, age-related cardiac dysfunction, postmenopausal osteoporosis, and ischemic stroke.
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- HY-110281
-
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Dehydroascorbic acid
|
490-83-5 |
99.94% |
|
Dehydroascorbic acid is an oxidized form of vitamin C that can cross the blood-brain barrier (BBB). Dehydroascorbic acid clears cytotoxic reactive oxygen species (ROS) produced after ischemic stroke by converting to ascorbic acid (AA), thereby reducing neuronal and glial cell damage and stabilizing cerebral microvascular NO signaling to maintain perfusion in the ischemic area. Dehydroascorbic acid can be used in research on ischemic stroke.
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- HY-125944
-
|
MitoTEMPO hydrate
|
1569257-94-8 |
98.03% |
|
MitoTEMPO hydrate is a mitochondria-targeted antioxidant. MitoTEMPO hydrate induces mitophagy by activating the PINK1/Parkin pathway, inhibits NLRP3 inflammasome activation, restores mitochondrial membrane potential, and improves renal function and podocyte injury. MitoTEMPO hydrate regulates Ca2+ homeostasis, inhibits Bnip3 overexpression, shortens action potential duration, and exerts antiarrhythmic effects. MitoTEMPO hydrate reverses premature senescence, reduces trabecular bone loss, and decreases cell apoptosis. MitoTEMPO hydrate can be used in studies of chronic kidney disease, age-related cardiac dysfunction, postmenopausal osteoporosis, and ischemic stroke.
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- HY-N2026
-
|
Propylparaben
|
94-13-3 |
99.96% |
|
Propylparaben (Propyl parahydroxybenzoate) is an antibacterial preservative that can be produced by plants and bacteria. Propylparaben is an orally active weak estrogen receptor agonist. Propylparaben regulates the PI3K-AKT and JNK signaling pathways, and induces oxidative stress. Propylparaben is commonly used in cosmetics, pharmaceuticals and foods, and can be used in studies related to ovarian aging and myocardial ischemia-reperfusion injury.
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- HY-108448
-
|
N-Oleoyldopamine
|
105955-11-1 |
99.47% |
|
N-Oleoyldopamine (OLDA) is an orally active TRPV1 activator and 5-LOX inhibitor with blood-brain barrier permeability. N-Oleoyldopamine excites histaminergic neurons in the tuberomammillary nucleus via a dopamine receptor mechanism, a process independent of TRPV1 and cannabinoid receptors. On one hand, N-Oleoyldopamine promotes the release of insulin and glucose-dependent insulinotropic polypeptide through a GPR119-dependent pathway to improve glucose tolerance; on the other hand, N-Oleoyldopamine improves left ventricular function and reduces myocardial infarction size by triggering the release of substance P and calcitonin gene-related peptide. N-Oleoyldopamine is used in studies related to glycemic abnormalities and myocardial ischemia-reperfusion injury.
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- HY-184089
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ATB1071
|
2921556-65-0 |
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ATB1071 is a brain-penetrant and orally active p62/SQSTM1 activator. ATB1071 binds to the p62-ZZ domain, promotes PB1-dependent p62 self-polymerization, and activates p62-mediated mitophagy. ATB1071 can be used for the research of Leigh syndrome, cerebral ischemia-reperfusion injury[1].
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- HY-175599A
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Z6466608628 hydrochloride
|
|
99.25% |
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Z6466608628 hydrochloride is a selective PPIL4 molecular glue degrader with human PPIL4 EC50 values of 0.34 µM. Z6466608628 hydrochloride functionally recruits PPIL4 to CRBN, induces CRL4CRBN-mediated ubiquitylation and degradation of PPIL4. Z6466608628 hydrochloride can be used for the research of intracranial aneurysms[1].
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- HY-180807
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MAPK-IN-6
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|
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MAPK-IN-6 (compound 116B) is a CNS-penetrant compound that inhibits the MAPK signaling pathway. MAPK-IN-6 reduces oxidative stress in SH-SY5Y neuronal cells by reducing ROS, restoring mitochondrial function, and inhibiting MAPK-driven inflammation. MAPK-IN-6 demonstrates profound neuroprotective efficacy in a rat tBCCAO/R model via ERK-P38-JNK signaling. MAPK-IN-6 can be used as a neuroprotective agent in ischemic stroke research.
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- HY-P10638
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TAT-CN21
|
|
99.38% |
|
TAT-CN21 is a potent CaMKII inhibitor with an IC50 of 77.2 nM. TAT-CN21 inhibits both calcium/calmodulin-dependent and autonomously activated CaMKII, blocks glutamate-induced translocation of CaMK IIα, and reverses the enhanced phosphorylation of CaMKII at Thr286 following excitotoxic injury. TAT-CN21 shows application potential in studies related to ischemic stroke by reducing neuronal excitotoxicity and exacerbating pre-existing long-term neuronal death prior to injury. TAT-CN21 improves definitive behaviors in rats with residual nerve injury without altering indicators such as mechanical/thermal hyperalgesia or spatial memory. TAT-CN21 can also be used in studies related to neuropathic pain.
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- HY-106950
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Fosfructose
|
488-69-7 |
98.0% |
|
Fosfructose is an orally active cyclooxygenase-2 inhibitor and Toll-like receptor 4 modulator. Fosfructose reduces the expression of cyclooxygenase-2, thereby decreasing prostaglandin production. By inhibiting the Toll-like receptor 4 signaling pathway, Fosfructose downregulates LPS-induced adhesion molecule expression. Fosfructose is applicable to research related to ischemic stroke, epilepsy, sepsis, myocardial injury, osteoporosis, and ultraviolet B-induced skin damage.
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- HY-173591
-
|
T0080
|
2785323-68-2 |
99.94% |
|
T0080 is a central nervous system-penetrant FPR1 inhibitor. By functionally blocking the FPR1 signaling pathway, T0080 effectively reduces neutrophil infiltration into ischemic brain tissue and maintains the integrity of the blood-brain barrier. T0080 alleviates tPA-associated hemorrhagic transformation, inhibits demyelination responses and the expression of NOX2. T0080 also possesses anti-apoptotic (apoptosis) and anti-inflammatory properties, thereby protecting myelin and reducing neurological deficits. T0080 is widely used in studies related to ischemic stroke complicated by hemorrhagic transformation after tPA thrombolysis, as well as multiple sclerosis.
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- HY-N2484
-
|
Methylnissolin
|
73340-41-7 |
99.92% |
|
Methylnissolin (Astrapterocarpan) is an osteoclast inhibitor with anti-inflammatory, neuroprotective and antioxidant activities. Methylnissolin downregulates the activation of the MAPK and PI3K/AKT pathways, inhibits the phosphorylation of MAPK1 and AKT1, and blocks PDGF-BB-induced phosphorylation of ERK1/2. Methylnissolin reduces the expression and secretion of proinflammatory mediators, decreases intracellular ROS levels, upregulates antioxidant enzymes, and downregulates osteoclastogenesis markers. Methylnissolin is applicable to research related to ischemic stroke, osteoporosis, cardiovascular diseases, skin aging, etc.
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- HY-14668
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|
Lomitapide mesylate
|
202914-84-9 |
99.61% |
|
Lomitapide (AEGR-733; BMS-201038) mesylate is an orally active microsomal triglyceride transfer protein (MTP) inhibitor and a selective mTORC1 inhibitor with lipid-lowering activity and BBB permeability. Lomitapide mesylate significantly reduces plasma LDL levels by blocking the assembly and secretion of very-low-density lipoprotein (VLDL). Lomitapide mesylate inhibits mTORC1 in an ATP-dependent manner, thereby inducing AMPK-independent autophagic cell death and suppressing cancer cell growth and apoptosis. Lomitapide mesylate also enhances tumor infiltration of CD8+ T cells. In addition, Lomitapide mesylate inhibits HDAC, improves endothelial function, effectively alleviates vascular inflammation and oxidative stress, and exerts neuroprotective effects in a cerebral ischemia/reperfusion injury model. Lomitapide mesylate can be used in research on related diseases such as colorectal cancer, breast cancer, melanoma, ischemic stroke, and familial hypercholesterolemia.
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- HY-N0334A
-
|
(+)-Magnoflorine iodide
|
4277-43-4 |
99.74% |
|
(+)-Magnoflorine (α-Magnoflorine) iodide is an orally active aporphine alkaloid with multiple biological activities. (+)-Magnoflorine iodide promotes Parkin/PINK1 -mediated mitochondrial autophagy, inhibits the activation of NLRP3/Caspase-1 pathway, regulates the intestinal microbiota, and exhibits significant anti-inflammatory and immunomodulatory activities. (+)-Magnoflorine iodide inhibits JNK and TLR4/NF-κB signaling pathways, activates Sirt1/AMPK pathway, alleviates neuronal oxidative stress and apoptosis. Magnoflorine upregulates miR-410-3p, inhibits HMGB1/NF-κB pathway, and has anti-tumor activity. (+)-Magnoflorine iodide also has significant antifungal activity.
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- HY-W011235
-
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Norfluoxetine hydrochloride
|
57226-68-3 |
99.58% |
|
Norfluoxetine hydrochloride is the active metabolite of the antidepressant Fluoxetine (HY-B0102); it is also a TREK-2 K2P potassium channel inhibitor. Norfluoxetine hydrochloride exhibits neuroimmunological activity, induces apoptosis in primary microglial cells, and inhibits the release of pro-inflammatory factors. Norfluoxetine hydrochloride inhibits high-threshold voltage-gated Ca2+ currents in neurons with an EC50 of 20.4 μM. Norfluoxetine hydrochloride can be used in research related to depression, ischemic stroke, and epilepsy.
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- HY-107661
-
|
Arundic Acid
|
185517-21-9 |
98.0% |
|
Arundic Acid is an orally effective astrocyte function modulator and neuroprotective agent. Arundic Acid increases the expression and function of the astrocytic glutamate transporter EAAT1 by activating the ERK, Akt and NF-κB pathways. Arundic Acid attenuates retinal ganglion cell death in a normal-tension glaucoma model. Arundic Acid exerts neuroprotective effects in a mouse model of Parkinson's disease. Arundic Acid is a S100β protein synthesis inhibitor that prevents neurological deficits and brain tissue damage after intracerebral hemorrhage in rats. Arundic Acid downregulates neuroinflammation and astrocytic dysfunction after status epilepticus in immature rats. Arundic Acid is applicable to research related to Parkinson's disease, cerebral ischemia, glaucoma, intracerebral hemorrhage and epilepsy.
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- HY-N0541
-
|
Pseudoginsenoside F11
|
69884-00-0 |
99.87% |
|
Pseudoginsenoside F11 is an orally active neuroprotective agent. Pseudoginsenoside F11 reduces the expression of β-amyloid precursor protein, inhibits the production of Aβ1-40, downregulates the expression of JNK2, p53 and activated Caspase 3, and restores the activities of SOD and Glutathione peroxidase. Pseudoginsenoside F11 inhibits the excessive activation of μ-Calpain and restores the level of neuronal Nitric oxide synthase. Pseudoginsenoside F11 reduces infarct volume, alleviates cerebral edema, decreases neuronal loss, improves neurological deficits and enhances long-term functional outcomes in transient cerebral ischemia models. Pseudoginsenoside F11 antagonizes Methamphetamine-induced behavioral deficits, dopamine level reduction and neurotoxicity without altering the baseline behaviors of normal mice. Pseudoginsenoside F11 can be used in studies related to Alzheimer's disease, transient cerebral ischemic injury and Methamphetamine-induced neurotoxicity.
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- HY-13769A
-
|
TPT-260 Dihydrochloride
|
2076-91-7 |
98.0% |
|
TPT-260 Dihydrochloride (NSC55712), a thiophene thiourea derivative, is a retromer complex stabilizer against thermal denaturation (Kd = ~5 µM). TPT-260 Dihydrochloride increases the levels of retromer proteins, shifts amyloid-precursor protein (APP) away from the endosome, and decreases the pathogenic processing of APP. TPT-260 Dihydrochloride inhibits TLR4 upregulation, IKKβ phosphorylation, NF-κB p65 nuclear translocation, and NLRP3 inflammasome formation. TPT-260 Dihydrochloride improves retromer-mediated cargo trafficking, reduces brain infarct area, and decreases amyloid plaque deposition. TPT-260 Dihydrochloride exhibits minimal cytotoxicity to primary microglia at tested concentrations. TPT-260 Dihydrochloride can be used for the research of inflammatory bowel disease, ischemic stroke and Alzheimer's disease.
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- HY-19820A
-
|
NSC45586 sodium
|
6300-44-3 |
98.0% |
|
NSC45586 sodium is an inhibitor of PHLPP. NSC45586 sodium targets the PP2C phosphatase domains of PHLPP1 and PHLPP2, blocks the phosphatase activity of PHLPP, increases the expression level of FOXO1 in the nucleus, and reduces the protein expression of PHLPP1. NSC45586 sodium activates the AKT survival signaling pathway, enhances IGF-1-induced AKT activation, and inhibits the phosphorylation of AKT/ERK under basal conditions. NSC45586 sodium reduces staurosporine-induced neuronal death, preserves notochord cell morphology and KRT19 expression, inhibits cell apoptosis (apoptosis), improves the viability and proliferation of nucleus pulposus cells, upregulates the expression of ACAN/SOX9, and downregulates the expression of MMP13. NSC45586 sodium binds tightly to bovine serum albumin (bovine serum albumin), and exerts a more significant effect on nucleus pulposus in male individuals. NSC45586 sodium can be used in studies related to global cerebral ischemia and intervertebral disc degeneration.
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-
- HY-W012352
-
|
2-Hydroxyanthraquinone
|
605-32-3 |
98.0% |
|
2-Hydroxyanthraquinone is a product generated by the photochemical oxidation of Anthracene (ANT) (HY-Y0299). 2-Hydroxyanthraquinone induces ferroptosis in cardiomyocytes by depleting GSH and inhibiting GPX4, leading to cardiac developmental malformations. 2-Hydroxyanthraquinone causes damage to the cerebrovascular system and blood-brain barrier in zebrafish by downregulating the Wnt/β-catenin signaling pathway, as well as inducing inflammation and neuronal apoptosis. 2-Hydroxyanthraquinone can be used in studies related to cerebrovascular diseases and cardiotoxicity.
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