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Targeted therapy! The Capetin Prize winning "Click Chemistry" can be used like this!Targeted therapy! The Nobel Prize winning "Click Chemistry" can be used like this!2025-02-06
802 Results for "
Vasodilator testing
" in MedChemExpress (MCE) Product Catalog:
Products (802)
802 Results for "Vasodilator testing" in MCE Product Catalog:
Cat. No.: HY-W107409
CAS No.: 213473-00-8
Category:
Target:
Cat. No.: HY-B1016R
CAS No.: 15421-84-8
Synonyms: AR-12008 (Standard)
Research Areas:
Trapidil (Standard) (AR-12008 (Standard)) is the analytical standard of Trapidil (HY-B1016R). This product is intended for research and analytical applications. Trapidil (AR-12008) is an orally active vasodilator and antiplatelet agent. Trapidil antagonizes platelet-derived growth factor (PDGF), inhibits phosphodiesterase, thromboxane A2 synthesis and pro-inflammatory cytokine production. Trapidil promotes prostacyclin biosynthesis, reduces lipid peroxidation, regulates nitric oxide metabolism, and inhibits cell proliferation and migration. Trapidil exerts tissue-protective effects, regulates bone turnover, and inhibits pyroptosis via the GPX3/Nrf2 pathway. Trapidil is applicable to research related to renal ischemia-reperfusion injury, chronic stable angina, restenosis, meningioma, diabetic cardiomyopathy and peripheral nerve crush injury.
Cat. No.: HY-B1035A
CAS No.: 47141-42-4
Synonyms: l-Bunolol
Research Areas:
Levobunolol (l-Bunolol) is a non-selective β-adrenergic antagonist and vasodilator. By blocking calcium ion influx and reducing the sensitivity of vascular smooth muscle to calcium, Levobunolol effectively dilates the ciliary arteries and increases ocular blood flow, so it is widely used in research on glaucoma and ocular hypertension. Levobunolol inhibits the β-receptor signaling pathway and the expression of related proliferation markers (such as CK3, CK14, CK19, Ki67) in corneal cells. In rabbit models, Levobunolol not only does not inhibit corneal epithelial regeneration, but also accelerates the healing of mechanical injury without adverse effects. Levobunolol also inhibits histamine-induced vasoconstriction and intracellular calcium elevation, exhibiting unique vascular regulatory activity. Levobunolol protects ocular blood flow and promotes corneal repair .
Cat. No.: HY-182366
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EED-IN-5 is an orally active, EZH2-selective trisubstituted pyridine-based EED-H3K27me3 inhibitor and immunomodulator with anti-inflammatory activity. The IC50 value of EED-IN-5 against EED is 28.21 nM. In mouse models, EED-IN-5 preferentially and persistently accumulates in lymph nodes after oral administration. By reducing the H3K27me3 level of dendritic cells and inhibiting their migration, EED-IN-5 decreases the infiltration of specific dendritic cells, macrophages and T cells into the spinal cord and brain. EED-IN-5 exhibits hERG inhibitory activity, shows negative results in the Mini-Ames test, and causes no obvious toxicity upon long-term high-dose administration. EED-IN-5 can be used for the research of multiple sclerosis .
Cat. No.: HY-N18124
CAS No.: 122688-84-0
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Cat. No.: HY-N19899
CAS No.: 910050-51-0
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Cat. No.: HY-19091
CAS No.: 123297-52-9
Research Areas:
ICI-170777 is an orally active cardiotonic agent and type III Phosphodiesterase inhibitor, with an IC50 of 2.5 μM against cyclic AMP phosphodiesterase type III from canine cardiac fractions. ICI-170777 inhibits Aldrin epoxidase and pentobarbital metabolism. It enhances β-adrenergic receptor-mediated positive inotropic effects without causing chronotropic effects, while also exerting balanced arteriolar/venular vasodilator, platelet aggregation inhibitor and smooth muscle relaxant activities. ICI-170777 restores cardiac function in an acute canine heart failure model, exhibits additive effects when combined with Ouabain (HY-B1457), and shows no significant activity against multiple receptor classes or non-cardiac systems. ICI-170777 can be used in research related to congestive heart failure .
Cat. No.: HY-U00134R
CAS No.: 2179-37-5
Synonyms: Bencyclane (Standard); Benzcyclan (Standard)
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Benzcyclane (Standard) is the analytical standard of Benzcyclane (HY-U00134). This product is intended for research and analytical applications. Benzcyclane (Bencyclane; Benzcyclan) is a vasodilator with serotonin receptor antagonism. Benzcyclane exerts atypical serotonin antagonistic effects in rabbit superior mesenteric arteries. Benzcyclane relaxes high K +-induced contractions in rabbit basilar arteries and superior mesenteric arteries, and selectively inhibits sympathetic nerve stimulation-induced contractions in rabbit pulmonary arteries. Benzcyclane exerts non-competitive norepinephrine antagonistic effects in rabbit superior mesenteric arteries, and slightly reduces the maximum contractile response induced by histamine. Benzcyclane relaxes smooth muscles, induces transient hypotension, inhibits thrombosis, and accelerates blood fibrinolytic activity. Benzcyclane increases cerebral glucose content/uptake, enhances hypoxia tolerance in mice, and increases cerebral blood supply in dogs. Benzcyclane is applicable to studies related to cerebral vascular circulation .
Cat. No.: HY-P991525
CAS No.: 2923542-55-4
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Cat. No.: HY-129440R
CAS No.: 68573-24-0
Cat. No.: HY-103117
CAS No.: 847871-78-7
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S 32212 hydrochloride is an inverse agonist of 5-HT receptors 5-HT2(CINI) and 5-HT2(CVSV) (Kis=6.6, 8.9 nM) and an antagonist of 5-HT2A and α2β-adrenergic receptors (Ki=5.8, 5.8 nM). S 32212 hydrochloride can reduce the binding of GTPγS to Gαq, and reduce the activity of phospholipase C (PLC) in HEK293 cells expressing 5-HT2(CINI) receptor and CHO cells expressing 5-HT2(CVSV) receptor (EC50=38 and 18.6 nM, respectively). S 32212 hydrochloride (2.5 mg/kg) reduces 5-HT receptor agonist-induced head twitches and penile erections in mice and rats. S 32212 hydrochloride (10, 40 mg/kg) reduces immobility time in the forced swim test and marble burying behavior in mice and rats, exerting antidepressant and anxiolytic activities.
Cat. No.: HY-129108
CAS No.: 205252-57-9
Synonyms: (9Z)-UAB-30
Research Areas:
9-cis-UAB30 is a rexinoid agonist. 9-cis-UAB30 significantly decreases the proliferation, viability, and motility of both patient-derived xenografts (PDXs). 9-cis-UAB30 induced cell-cycle arrest as demonstrated by the significant increase in the percentage of cells in G1 and a decrease in the percentage of cells in S phase by downregulating SKP2 and/or 20S proteasome activity, which leads to increased p27kip1 protein stability. 9-cis-UAB30 downregulates the abundance of stem cell marker mRNAs (Oct4, Nanog, Sox2, nestin) and upregulates the abundance of differentiation marker mRNAs (β3-tubulin, NSE, HOXC9, GAP43). 9-cis-UAB30 has no adverse effects on the central nervous system and cardiovascular system at the tested dose. 9-cis-UAB30 can be used for the study of neuroblastoma, cutaneous T-cell lymphomas, and breast cancer .
Cat. No.: HY-184337
CAS No.: 143111-84-6
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Dihydroparadol is a iNOS inhibitor with an IC50 of 7.24 μM, and it is found in ginger. Dihydroparadol partially inhibits the catalytic activity of iNOS, blocks the nuclear translocation of NF-κB p65, reduces NF-κB activity, and attenuates lipopolysaccharide-induced degradation of IκB-α, thereby inhibiting NF-κB-mediated iNOS gene expression and protein production. Dihydroparadol inhibits lipopolysaccharide-induced nitric oxide production in macrophages and exhibits anti-inflammatory activity. Dihydroparadol increases ABCA1 protein abundance by elevating mRNA levels and reducing proteasomal degradation, and also increases ABCG1 protein abundance by enhancing protein stability. Dihydroparadol promotes cholesterol efflux from cholesterol-loaded macrophages via apolipoprotein A1-mediated and plasma-mediated pathways. Dihydroparadol inhibits PDGF-induced vascular smooth muscle cell proliferation, shows no cytotoxicity to vascular smooth muscle cells within the tested concentration range, and does not interfere with endothelial cell proliferation. Dihydroparadol can be used in the research of inflammatory diseases, atherosclerosis and cardiovascular diseases .
Cat. No.: HY-W010736A
CAS No.: 40290-32-2
Cat. No.: HY-W011927
CAS No.: 80-09-1
Synonyms: Bisphenol S; Bis(4-hydroxyphenyl) sulfone
Cat. No.: HY-N22017
CAS No.: 2341324-20-5
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Cat. No.: HY-W075770
CAS No.: 1313-99-1
Synonyms: Nickel monoxide
Target:
Environmental Pollutants Apoptosis Reactive Oxygen Species (ROS) Caspase TGF-beta/Smad p38 MAPK Akt PI3K
Research Areas:
Nickel(II) oxide (nickel monoxide) is a chemical warfare agent that can enter the body through the respiratory tract and other routes, distributing to organs such as the lungs and testes. The nanoparticle form of nickel(II) oxide (NiO NPs) exhibits antibacterial, anti-leishmanial, anti-diabetic, and anti-cancer activities. NiO NPs can be activated by ultraviolet and visible light, generating reactive oxygen species (ROS). Nickel(II) oxide induces oxidative stress by generating reactive oxygen species, activating the TGF-β1-mediated MAPK and PI3K/AKT pathways, disrupting the MMPs/TIMPs balance, and upregulating the expression of inflammatory factors (IL-1β, IL-6) and apoptosis-related molecules (Bax, caspase-3, p53), while inhibiting the activity of the anti-apoptotic molecule Bcl-2. Nickel(II) oxide induces cytotoxicity, promotes fibrosis, triggers inflammatory responses, and causes apoptosis. Nickel(II) oxide can be applied in research on the safety assessment of nanomaterials, such as in the context of pulmonary fibrosis and reproductive system toxicity .
Cat. No.: HY-W011927R
CAS No.: 80-09-1
Synonyms: Bisphenol S (Standard); Bis(4-hydroxyphenyl) sulfone (Standard)
Cat. No.: HY-L076
641 compounds
Drug-induced liver injury (DILI; also known as drug-induced hepatotoxicity) is caused by medications (prescription or OTC), herbal and dietary supplements (HDS), or other xenobiotics that result in abnormalities in liver tests or in hepatic dysfunction that cannot be explained by other causes. Drugs are an important cause of liver injury. Drug-induced hepatic injury is the most common reason cited for withdrawal of an approved drug.
DILI is thought to occur via several different mechanisms. Among these are direct impairment of the structural (e.g., mitochondrial dysfunction) and functional integrity of the liver; production of a metabolite that alters hepatocellular structure and function; production of a reactive drug metabolite that binds to hepatic proteins to produce new antigenic drug-protein adducts, which are targeted by hosts’ defenses (the hapten hypothesis); and initiation of a systemic hypersensitivity response (i.e., drug allergy) that damages the liver.
MCE Drug-induced Liver Injury (DILI) Compound Library contains a unique collection of 641 hepatotoxicity causing compounds and is a powerful tool to research DILI and other drug toxicities. This library can be used to understand the mechanisms of DILI, identify biomarkers for early DILI prediction, and allow timely recognition during drug development, thus finally achieving successful DILI prevention and assessment in the pre-marketing phase.
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Protocols
Targeted therapy! The Capetin Prize winning "Click Chemistry" can be used like this!Targeted therapy! The Nobel Prize winning "Click Chemistry" can be used like this!A suitable model is crucial in drug screening experiments. Organs can mimic the three-dimensional functional structure of internal organs, have similar spatial organization to corresponding organs, maintain some key characteristics, and reproduce some physiological functions. They are widely used for modeling and personalized drug screening physiological functions.2025-02-06
