Brovincamine
Brovincamine is an orally active slow Ca2+ channel blocker and vasodilator. Brovincamine reduces Ca2+ influx across the plasma membrane by blocking Ca2+ channels. Brovincamine inhibits catecholamine secretion, cholinergic function, autonomic parasympathetic nervous system activity, cerebrovascular resistance, and nerve stimulation-induced convulsive responses. Brovincamine induces cerebrovascular, coronary, and intracranial vasodilation, improves cerebral cortical microcirculation, enhances cerebral metabolic activity, and increases capillary clearance efficiency. Brovincamine can be used in research related to cerebral ischemic diseases, cardiac ischemic diseases, and normal-tension glaucoma.
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- CAS. Nr.: 57475-17-9
- Formel: C21H25BrN2O3
- Molecular Weight:433.35
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Speicherung:
Please store the product under the recommended conditions in the Certificate of Analysis.
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Biologische Aktivität
Beschreibung
In Vitro
Brovincamine (30-100 μM; 10 min) inhibits Carbamoylcholine (HY-B1208)-induced (IC50 30 μM) and high K+-induced (IC50 100 μM) catecholamine secretion and calcium influx in cultured bovine adrenal chromaffin cells, and its inhibitory characteristics vary with extracellular Ca2+ concentration depending on the secretagogue[1].
MedChemExpress (MCE) has not independently confirmed the accuracy of these methods. They are for reference only. Further protocols information, click here.
In Vivo
Brovincamine (2-4 mg/kg, intravenous injection; single/cumulative administration) slightly but dose-dependently inhibits ganglionic stimulant-induced tachycardia in spinal dogs[2].
Brovincamine (7.5 mg/kg/day; p.o.; daily administration; for 4 weeks) improves cortical cerebral capillary morphology in young adult rats and aged healthy rats by increasing the volume, length, and density of cortical cerebral capillaries while decreasing capillary diameter and intercapillary distance[4].
MedChemExpress (MCE) has not independently confirmed the accuracy of these methods. They are for reference only.
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Animal Model:Mongrel dogs (either sex, weighing 6-12 kg, spinal model)[2]
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Dosage:6.4 mg/kg
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Administration:i.v.; single dose
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Result:Slightly inhibited the increases in blood pressure and heart rate induced by i.v. DMPP.
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Animal Model:Mongrel dogs (either sex, weighing 6-12 kg, spinal model)[2]
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Dosage:2 mg/kg; 4 mg/kg
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Administration:i.v.; single dose; cumulative
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Result:Induced a slight but stepwise inhibition of tachycardia elicited by DMPP, BCH, and AT II delivered to cardiac sympathetic ganglia.
Significantly reduced positive chronotropic responses to AT II.
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Animal Model:OFA (Sprague Dawley) (female; 12 months, 36 months)[4]
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Dosage:7.5 mg/kg/day
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Administration:p.o.; daily; 4 weeks
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Result:Reduced capillary diameter from 3.20 μm to 2.97 μm in 12-month-old rats.
Increased capillary volume fraction from 3.62% to 4.46% in 12-month-old rats.
Reduced mean intercapillary distance from 30.90 μm to 27.79 μm in 12-month-old rats.
Increased capillary length per unit cortex from 54.87 cm/mm3 to 69.03 cm/mm3 in 12-month-old rats.
Increased number of capillaries per measuring field from 20 to 23 in 12-month-old rats.
Reduced capillary diameter from 3.29 μm to 3.09 μm in 36-month-old rats.
Increased capillary volume fraction from 3.67% to 4.45% in 36-month-old rats.
Reduced mean intercapillary distance from 31.04 μm to 28.78 μm in 36-month-old rats.
Increased capillary length per unit cortex from 50.77 cm/mm3 to 71.15 cm/mm3 in 36-month-old rats.
Increased number of capillaries per measuring field from 19 to 23 in 36-month-old rats.
Chemical Information
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CAS. Nr. 57475-17-9
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Molecular Weight 433.35
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Formel C21H25BrN2O3
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SMILES
C(C)[C@]12[C@]3(C=4N(C=5C(C4CCN3CCC1)=CC=C(Br)C5)[C@](C(OC)=O)(O)C2)[H]
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Versand
Room temperature in continental US; may vary elsewhere.
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Speicherung
Please store the product under the recommended conditions in the Certificate of Analysis.
Protokoll
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Protocol for Pharmacokinetic Study
Pharmacokinetic studies quantify how an organism handles a drug over time through absorption, distribution, metabolism, and excretion, and the core experimental readout is the concentration-time profile of parent drug and, when relevant, metabolites in biological matrices such as plasma, whole blood, urine, bile, or tissue. Pharmacokinetic analysis links dose, route, exposure, clearance, half-life, distribution, bioavailability, and systemic exposure to drug efficacy and toxicity hypotheses rather than measuring a signaling pathway directly. The literature links pharmacokinetics to drug-development phenotypes by showing that drug metabolism and pharmacokinetics influence compound progression, exposure-response interpretation, safety margins, dosing strategy, and failure risk during discovery and development. DMPK science contributes to compound optimization by integrating physicochemical properties, in vitro metabolism, transporter behavior, in vivo exposure, and pharmacodynamic contex
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Ca2+ Staining Technique
Ca2+ staining is an experimental technique that utilizes specific fluorescent probes (such as Fluo-4 AM, Fura-2, etc.) to qualitatively or quantitatively detect dynamic changes in intracellular Ca2+ concentrations; this is achieved by monitoring the changes in fluorescent signals generated when these probes bind to free intracellular calcium ions. The underlying principle relies primarily on the presence of chelating groups within the probe's molecular structure that possess high affinity for calcium ions.
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MTT Cell Proliferation Assay
The MTT assay is a colorimetric endpoint assay for estimating viable cell number, cell growth, cytotoxicity, or cell activation in cultured mammalian cells. Living cells reduce the yellow tetrazolium salt MTT into purple/blue formazan, while dead cells do not generate the same signal; the resulting color can be quantified with a multiwell spectrophotometer. MTT reduction is commonly interpreted as a readout of metabolic activity that often correlates with viable cell number, but it should not be treated as a direct cell-counting method unless the assay is optimized for the cell type and experimental condition. Studies show that MTT reduction can involve mitochondrial and non-mitochondrial reducing systems, and formazan may accumulate in intracellular lipid droplets rather than simply marking mitochondria.
Reinheit & Dokumentation
Verweise
Calculators
Konzentration (Stammlösung) × Volumen (Stammlösung) = Konzentration (Ziellösung) × Volumen (Ziellösung)