Detail of > 61-76-7
- MSDS Download

- CAS Number:
- 61-76-7
- Name:
Benzenemethanol, 3-hydroxy-α-[(methylamino)methyl]-,hydrochloride (1:1), (aR)-
- Superlist Name:
- Phenylephrine hydrochloride
- Formula:
- C9H14ClNO2
- Molecular Structure:
![Molecular Structure of 61-76-7 (Benzenemethanol, 3-hydroxy-α-[(methylamino)methyl]-,hydrochloride (1:1), (aR)-)](http://www.lookchem.com/300w/2010/0623/61-76-7.jpg)
- Synonyms:
- L(-)-Phenylephrine hydrochloride;(R)-(-)-1-(3-Hydroxyphenyl)-2-methylaminoethanol hydrochloride;3-Hydroxy-alpha-(methylaminomethyl)benzyl alcohol;
- Molecular Weight:
- 203.6
- EINECS:
- 200-517-3
- Melting Point:
- 143-145 °C(lit.)
- Boiling Point:
- 341.1 °C at 760 mmHg
- Flash Point:
- 163.4 °C
- Appearance:
- white to almost white crystalline powder
- Hazard Symbols:
Xn- Risk Codes:
- 22-36/37/38
- Safety:
- 26-36-37/39Details
- Transport Information:
- UN 3249
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Reference
- Adrenergic receptor mechanisms involved in the hyperglycemia and hyperlacticacidemia produced by sympathomimetic amines in the cat
- Adrenergic receptor mechanisms involved in the hyperglycemia and hyperlacticacidemia produced by sympathomimetic amines in the cat. Kuo, Shu-Hui; Kamaka, Joseph K.; Lum, Bert K. B. (John A. Burns Sch. Med., Univ. Hawaii, Honolulu, Hawaii, USA). J. Pharmacol. Exp. Ther., 202(2), 301-9 (English) 1977. CODEN: JPETAB. DOCUMENT TYPE: Journal CA Section: 2 (Hormone Pharmacology) Dose-related increases in blood glucose were produced by the infusion of l-isoproterenol bitartrate [54750-10-6], phenylephrine-HCl [61-76-7], and epinephrine bitartrate (I bitartrate) [51-42-3] in the cat. The hyperglycemic response to isoproterenol was blocked by propranolol but not by phenoxybenzamine; the converse was true in terms of blockade of the hyperglycemic response to phenylephrine. Blockade of the hyperglycemia induced by I required the combined admnistration of both propranolol and phenoxybenzamine. The hyperglycemic response to phenylephrine was largely unaffected by acute pancreatectomy. Both isoproterenol and phenylephrine stimulated the release of glucose from the isolated perfused cat liver prepn. Apparently, both .alpha. and .beta. receptors can mediate adrenergically induced hyperglycemic and hepatic glycogenolytic responses in the cat. In contrast, the hyperlacticacidemia induced by sympathomimetics in the cat, was solely mediated by .beta. receptors as evident by the observations that phenylephrine failed to elevate blood lactate [50-21-5], and the hyperlacticacidemia produced by I was blocked by propranolol and not by phenoxybenzamine. H35/25 and propranolol effectively antagonized both the hyperglycemia and hyperlacticacidemia induced by isoproterenol whereas practolol failed to antagonize the hyperglycemia and only moderately reduced the hyperlacticacidemia. These latter results suggest that both the hyperlacticacidemic response and the .beta. component of the hyperglycemic response to adrenergic agents are mediated by the .beta.-2 receptor subtype.
- Effect of Bronkosol and its components on cardiopulmonary parameters in asthmatic patients
- Effect of Bronkosol and its components on cardiopulmonary parameters in asthmatic patients. Spector, Sheldon L.; Hudson, Leonard; Petty, Thomas L. (Med. Cent., Univ. Colorado, Denver, Colo., USA). J. Allergy Clin. Immunol., 59(5), 371-6 (English) 1977. CODEN: JACIBY. DOCUMENT TYPE: Journal CA Section: 1 (Pharmacodynamics) Bronkosol [63550-80-1] and its components, isoetharine-HCl (I) [50-96-4] and phenylephrine-HCl (II) [61-76-7] hydrochloride, were compared in a double-blind randomized fashion for their effect on pulmonary and cardiovascular parameters in patients with reversible bronchospasm. Bronkosol and I produced bronchodilation as measured by forced expiratory vol. in 1 sec. (FEV1), forced vital capacity (FVC), and mean forced expiratory flow during the middle half of the FVC (isovol. FEF 25% to 75%), and II did not. There was no difference between Bronkosol and I in the degree of duration of bronchodilation. More patients had to discontinue after 15 min on the day of testing with II than with Bronkosol or I. Heart rate was no increased after Bronkosol or I, confirming its selective beta-2-action. The addn. of II to I had no beneficial effect on O satn. There was no difference between these drugs in systolic and diastolic blood pressure, pulse, or respiration. The results cast doubt on the useful contribution of II in Bronkosol.
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