Detail of > 38304-91-5
- MSDS Download

- CAS Number:
- 38304-91-5
- Name:
Minoxidil
- Formula:
- C9H15N5O
- Molecular Structure:

- Synonyms:
- Mimosine;Minoxidil(USP 24);Minoxidil USP/BP;Loniten (TN);U-10,858;2,4-Diamino-6-piperidinopyrimidine 3-N-oxide;Prexidil;6-Amino-1,2-dihydro-1-hydroxy-2-imino-4-piperidinopyrimidine;Alopexil;U 10858;Regaine;Minossidile [Italian];Prestwick_521;Minoximen;2,4-Pyrimidinediamine, 6-(1-piperidinyl)-, 3-oxide;Loniten;2,3-Dihydro-3-hydroxy-2-imino-6-(1-piperidinyl)-4-pyrimidinamine;Minoxidilum [INN-Latin];Pyrimidine, 2,4-diamino-6-piperidino-, 3-oxide;Minoxidil (USP);PDP;Tricoxidil;6-(1-Piperidinyl)-2,4-pyrimidinediamine 3-oxide;2,6-Diamino-4-piperidinopyrimidin-1-oxid;Rogaine;Alostil;3-hydroxy-2-imino-6-(1-piperidyl)pyrimidin-4-amine;6-Piperidino-2,4-diaminopyrimidine 3-oxide;2,4-Pyrimidinediamine,6-(1-piperidinyl)-,3- oxide;2,4-Diamino-6-piperidinopyrimidine 3-oxide;2,4-Diamino-6-piperidinilpirimidina-3-ossido [Italian];Theroxidil;4-Pyrimidinamine, 2,3-dihydro-3-hydroxy-2-imino-6-(1-piperidinyl)-;
- Molecular Weight:
- 209.29
- EINECS:
- 253-874-2
- Density:
- 1.52 g/cm3
- Melting Point:
- 272-274 °C (dec.)(lit.)
- Boiling Point:
- 351.7 °C at 760 mmHg
- Flash Point:
- 166.5 °C
- Appearance:
- White crystalline powder
- Hazard Symbols:
Xn,
T+- Risk Codes:
- 22-36/37/38-26/27/28
- Safety:
- 26-36-45-36/37/39-22Details
- Deleted CAS:
- 16317-69-4
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Reference
- Minoxidil in resistant hypertension
- Minoxidil in resistant hypertension. Dargie, H. J.; Dollery, C. T.; Daniel, J. (Dep. Clin. Pharmacol., R. Postgrad. Med. Sch., London, Engl.). Lancet, 8037, 515-18 (English) 1977. CODEN: LANCAO. DOCUMENT TYPE: Journal CA Section: 1 (Pharmacodynamics) Minoxidil (I) [38304-91-5], in combination with propranolol [525-66-6] and the diuretic frusemide [54-31-9], controlled the blood pressure in a group of hypertensive patients who were resistant to treatment with larges doses of std. drugs. The main problem was fluid retention, but subjective side effects were fewer than in a comparable group on other drugs.
- Vasodilators and ventricular septal defect: comparison of prazosin, minoxidil, and hydralazine in a chronic lamb model
- Vasodilators and ventricular septal defect: comparison of prazosin, minoxidil, and hydralazine in a chronic lamb model. Boucek, Mark M.; Chang, Richard; Synhorst, David P. (Coll. Med., Univ. Utah, Salt Lake City, UT 84132, USA). Pediatr. Res., 18(9), 859-64 (English) 1984. CODEN: PEREBL. ISSN: 0031-3998. DOCUMENT TYPE: Journal CA Section: 1 (Pharmacology) The vol. overloading of the left ventricle which results from left to right (L-R) shunting through a ventricular septal defect (VSD) may be reduced by pharmacol. agents which lower systemic vascular resistance (Rs) in excess of pulmonary arteriolar vascular resistance (Rpa). To study agents capable of decreasing the L-R shunt through systemic vasodilation, a chronic lamb model with VSD was created, to which three vasodilators, prazosin [19216-56-9] (0.05 mg/kg), hydralazine [86-54-4] (0.75 mg/kg), and minoxidil [38304-91-5] (0.25 mg/kg), were administered. Prazosin increased the Rpa while lowering Rs, resulting in an increase in Rpa/Rs, by 43% (p £ 0.005). Prazosin decreased the pulmonary flow (Qp) slightly, decreased L-R shunt by 16%, reduced the pulmonary to systemic flow ratio (Qp/Qs) by 22% (p £ 0.005), and lowered the left atrial mean pressure (LA) by 16% (p £ 0.005) with no effect on heart rate. Hydralazine lowered the Rpa and Rs equally and thus did not change the Rpa/Rs or the vol. of L-R shunt (7.6 vs. 8.1 L/min/m2). No change in LA was seen with hydralazine but heart rate increased from 162 to 200/min (p £ 0.01). Minoxidil did not change the L-R shunt (6.9 vs. 6.8 L/min/m2) and, in general, produced effects intermediate between prazosin and hydralazine. The data support a selective systemic vasodilation with prazosin, a property not shared by either minoxidil or hydralazine, which results in a redn. of shunting and left ventricular vol. overloading in lambs with VSD. Furthermore, since prazosin did not decrease the pulmonary resistance, the data indicate that the elevation in pulmonary resistance in lambs with VSD is not mediated by the a1-adrenergic receptor.
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