Losulazine
Based on 1 Customer Validation
Losulazine is an orally active antihypertensive agent. Losulazine modulates acid phosphatase, 3β-hydroxysteroid dehydrogenase, and 17β-hydroxysteroid dehydrogenase activity. Losulazine can be used for the research of hypertension.
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- Purity : 98.83%
- CAS No.: 72141-57-2
- 화학식: C27H22F4N4O3S
- 분자량:558.55
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보관:Powder -20°C, 3 years , 4°C, 2 years ; In solvent -80°C, 6 months , -20°C, 1 month
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Biological Activity
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Chemical Information
- Protocol
- 순도&문서
- References
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Help & FAQs
Biological Activity
제품 설명
In Vivo
Losulazine (4-32 mg/kg; p.o.; daily; 1 year or 30 weeks) induces dosage-dependent reversible decreased fertility, dosage-dependent reduced body weight gain and food consumption, non-dosage-related minimal to mild testicular lesions, and increased relative organ weights in male Sprague-Dawley rats[2].
Losulazine (10 mg/kg; p.o.; single dose or daily for 15-27 days) causes complete anestrus in female Sprague-Dawley rats via hypothalamic catecholamine depletion and subsequent hyperprolactinemia[3].
Losulazine (2-8 mg/kg; p.o.; daily) dose-dependently impairs fertility and reproductive performance in both sexes of Sprague-Dawley rats[4].
Losulazine (2.5-10 mg/kg; i.p.; single dose) produces marked, sustained catecholamine depletion in brain and pituitary regions outside the blood-brain barrier, with modest, transient dopamine reductions in barrier-protected regions, and increases plasma prolactin and α-melanocyte-stimulating hormone concentrations transiently in rats[5].
Losulazine (2.5 mg/kg; i.p.; single dose; or daily for 12 days) causes estrous cycle disruption in female rats, produces sustained catecholamine depletion in barrier-free brain and pituitary regions without tolerance, and has cumulative dopamine-depleting effects in the striatum, while sparing central 5-hydroxytryptaminergic neurons[5].
Losulazine exerts hypotensive activity in conscious monkeys by modulating sympathetic nerve activity without causing orthostatic hypotension[6].
MedChemExpress (MCE) has not independently confirmed the accuracy of these methods. They are for reference only.
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Animal Model:Wistar rats (adult male, 120-140 days old, 145-170 g)[1]
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Dosage:1; 2; 5 mg/kg
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Administration:i.p.; daily; 13 days
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Result:Significantly increased relative weights of total prostate, ventral prostate, and seminal vesicles at all doses.
Significantly increased relative coagulating gland weight only at 2 mg/kg.
Caused no significant changes in relative testes or epididymis weights.
Significantly increased testicular 3β-hydroxysteroid dehydrogenase (HSD) and 17β-HSD activity, while reducing testicular cholesterol content.
Significantly increased testicular acid phosphatase activity, ventral prostate acid phosphatase activity, and fructose content in seminal vesicles at 1 and 2 mg/kg.
Significantly reduced testicular acid phosphatase activity, and fructose content in seminal vesicles at 5 mg/kg.
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Animal Model:Sprague-Dawley rats (male, 220-358 g)[2]
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Dosage:4; 8; 16; 32 mg/kg
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Administration:p.o.; daily; 1 year or 30 weeks
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Result:Induced dosage-dependent ptosis, somnolence, fecal softening/decreased food consumption.
Caused statistically significant decreased body weight gain in the 16 and 32 mg/kg; retarded weight gain occurred only in the second half of the study in the 8 mg/kg group.
Decreased urinary pH in the 8, 16, and 32 mg/kg/day groups; no biologically significant changes in urinalysis values between treated and control rats.
Lowered luteinizing hormone levels significantly to 3.3 ng/mL in the 32 mg/kg/day group; no significant changes in prolactin or testosterone levels were seen in any treated group.
Increased relative spleen, heart, and adrenal weights in all treated groups.
Increased relative brain weights.
Produced dosage- and time-dependent decreased conception rates during treatment.
Promoted significant fertility recovery within 5 weeks of drug withdrawal, with no significant differences between treated and control groups.
Increased incidence of epididymal degenerate cells in all groups.
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Animal Model:Sprague-Dawley rats (female, 210 to 270 g) with reproductive dysfunction[3]
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Dosage:10 mg/kg
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Administration:p.o.; single dose or daily for 15, 16, 27 days
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Result:Reduced hypothalamic dopamine, norepinephrine, and epinephrine.
Depleted hypothalamic dopamine, norepinephrine, and epinephrine.
Reduced uterus-cervix-vagina weights and caused vaginal mucosa attenuation with vacuolated surface epithelium, and caused splenic congestion.
Did not affect serum follicle-stimulating hormone, luteinizing hormone, and progesterone levels.
Induced partial ptosis and fecal softening as clinical signs.
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Animal Model:Sprague-Dawley (Upj: TUC(SD)spf; male and female; 8-10 weeks of age, males 220-361 g, females 209-270 g at study start)[4]
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Dosage:2; 4; 8 mg/kg
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Administration:p.o.; daily
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Result:Caused ptosis in all treated rats.
Increased mean body weight gain in treated females after 14 days of treatment.
Disrupted estrous cycles in treated females, with significantly more days in diestrus, fewer days in proestrus, estrus, metestrus, and fewer total cycles over 14 days of treatment.
Decreased conception rates dose-dependently.
Prolonged mean gestation lengths in treated females given 4 and 8 mg/kg.
Induced moderate to severe testicular tubular necrosis, spermatic giant cell formation, and tubular atrophy in treated males.
Caused exudative prostatitis and ampullary gland sperm granulomas in 2, 4, 8 mg/kg groups.
Delayed functional development.
Reduced negative geotaxis response scores and prolonged response times at multiple time points in treated groups.
Impaired reproductive ability of F1 offspring.
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Animal Model:Long-Evans rats (adult male, 200-225 g)[5]
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Dosage:2.5; 5; 10 mg/kg
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Administration:i.p.; single dose
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Result:Produced maximal depletion of dopamine and norepinephrine in the median eminence, intermediate lobe, and neural lobe.
Reduced dopamine concentrations in the striatum and nucleus accumbens.
Reduced dopamine levels in the dorsomedial nucleus.
Failed to reduce norepinephrine concentrations in the dorsomedial nucleus.
Caused no effect on 5-hydroxytryptamine concentrations in the dorsomedial nucleus.
Increased plasma prolactin and α-melanocyte-stimulating hormone levels.
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Animal Model:Long-Evans (adult female, 200-225 g, regular estrous cycles prior to treatment)[5]
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Dosage:2.5 mg/kg
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Administration:i.p.; single dose; or daily for 12 days
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Result:Caused rats to become acyclic with persistent diestrous-like smears by 6-7 days of chronic treatment.
Produced 80-90% dopamine depletion and 50-70% norepinephrine depletion in the median eminence, intermediate lobe, and neural lobe with both acute and chronic doses, with no tolerance development.
Caused greater dopamine depletion in the striatum with chronic administration than acute administration, with a nonsignificant trend toward greater depletion in the nucleus accumbens.
Produced modest decreases in dopamine and norepinephrine concentrations in the dorsomedial nucleus with both acute and chronic doses, with no effect on 5-hydroxytryptamine concentrations in this region.
Chemical Information
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CAS No. 72141-57-2
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Appearance Solid
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분자량 558.55
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화학식 C27H22F4N4O3S
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Color Light yellow to light brown
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SMILES
O=C(N1CCN(S(=O)(C2=CC=C(C=C2)F)=O)CC1)C3=CC=C(NC4=C5C=CC(C(F)(F)F)=CC5=NC=C4)C=C3
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선적
Room temperature in continental US; may vary elsewhere.
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보관
Powder -20°C 3 years 4°C 2 years In solvent -80°C 6 months -20°C 1 month
Protocol
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Research Protocol for Cardiovascular Diseases
Cardiovascular disease can be modeled as maladaptive cardiac remodeling, where ischemic injury or pressure overload activates inflammatory signaling, fibroblast activation, extracellular-matrix deposition, cardiomyocyte hypertrophy, vascular remodeling, and progressive ventricular dysfunction. The TGF-β/SMAD axis is a central profibrotic pathway after myocardial injury and pressure overload, while innate immune and cytokine pathways regulate leukocyte recruitment, scar formation, and adverse remodeling. Key unresolved questions include which inflammatory signals are reparative versus harmful, when fibrosis is protective versus maladaptive, and whether pathway inhibition improves function without weakening necessary infarct healing or compensatory remodeling.
순도&문서
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Data Sheet (284 KB)
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SDS (251 KB)
- English - EN (251 KB)
- Français - FR (251 KB)
- Deutsch - DE (251 KB)
- Norwegian - NO (251 KB)
- Español - ES (251 KB)
- Swedish - SV (251 KB)
- Italian - IT (251 KB)
- Korean - KR (251 KB)
- Portuguese - PT (251 KB)
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Handling Instructions (2659 KB)
References
[1]. Ray A, et al. Study on the activities of testes and accessory sex glands after losulazine treatment in rats. Toxicol Lett. 1994 Sep;73(3):175-83. [Content Brief]
[5]. Pan JT, et al. Comparison of the effects of losulazine and reserpine on central aminergic neurons. Toxicol Appl Pharmacol. 1993 Nov;123(1):26-33. [Content Brief]
[6]. Gore R, et al. Losulazine, a new antihypertensive. Clin Pharmacol Ther. 1985 Aug;38(2):195-8. [Content Brief]
Calculators
Concentration (start) × Volume (start) = Concentration (final) × Volume (final)
Losulazine Related Classifications
HY-106447 Related Classifications
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