(-)-Phenylephrine

167.21

167.21

200-424-8

1WS297W6MV

DTXSID9023465

C62067

S01|S01FB01|C - Cardiovascular system|R - Respiratory system|S - Sensory organs

52.5

-0.31

Solid

1.159 g/cm3

169-172 °C

341.1ºC at 760 mmHg

163.4ºC

-55.5 ° (C=5, 1mol/L HCl)

Freely soluble in water;In water, 1X10+6 mg/L at 25 deg C (est)

Store below 40 deg C (104 deg F), preferably between 15 and 30 deg C (59 and 86 deg F), unless otherwise specified by manufacturer. Store in a tight, light-resistant container if not more than 15 mL size. Protect from freezing.

2.2X10-15 mm Hg at 25 deg C (est)

LD50 oral in rat: 350mg/kg

8.97None

Henry's Law constant = 6.8X10-15 atm-cu m/mol at 25 °C (est)

8.97|pKa = 8.97

CRYSTALS; BITTER; MP: 140-145 °C; FREELY SOL IN WATER OR ALCOHOL; SPECIFIC OPTICAL ROTATION: -46.2 TO -47.2 DEG @ 25 °C/D; AQ SOLN IS NEUTRAL TO LITMUS PAPER /PHENYLEPHRINE HYDROCHLORIDE/|WHITE TO OFF-WHITE, CRYSTALLINE POWDER; PKA: 7.6 /PHENYLEPHRINE HYDROCHLORIDE/|ODORLESS, /PHENYLEPHRINE HYDROCHLORIDE/|Hydroxyl radical reaction rate constant = 1.6X10-10 cu cm/molec-sec at 25 °C (est)

22-36/37/38-41-37/38

26-36-45-39

DO7175000

Xn

Prolonged exposure to air or strong light may cause oxidation and discoloration.

P261, P264, P270, P271, P272, P280, P285, P301+P312, P302+P352, P304+P312, P304+P340, P304+P341, P305+P351+P338, P312, P321, P322, P330, P333+P313, P337+P313, P342+P311, P363, P403+P233, P405, P501

H302

SRP: At the time of review, criteria for land treatment or burial (sanitary landfill) disposal practices are subject to significant revision. Prior to implementing land disposal of waste residue (including waste sludge), consult with environmental regulatory agencies for guidance on acceptable disposal practices.

The Approved Drug Products with Therapeutic Equivalence Evaluations List identifies currently marketed prescription drug products, incl phenylephrine hydrochloride, approved on the basis of safety and effectiveness by FDA under sections 505 of the Federal Food, Drug, and Cosmetic Act. /Phenylephrine Hydrochloride/|Drug products containing certain active ingredients offered over-the-counter (OTC) for certain uses. A number of active ingredients have been present in OTC drug products for various uses, as described below. However, based on evidence currently available, there are inadequate data to establish general recognition of the safety and effectiveness of these ingredients for the specified uses: phenylephrine hydrochloride (less than 0.08 percent) is included in ophthalmic vasoconstrictor drug products. /Phenylephrine hydrochloride/|Nasal decongestant active active ingredients. The active ingredient of the product consists of any of the following when used in the dosage limits and in the dosage forms established for each ingredient. Oral nasal decongestants: phenylephrine hydrochloride, phenylephrine bitartrate in an effervescent dosage form. Topical nasal decongestants: Phenylephrine hydrochloride. /Phenylephrine hydrochloride; Phenylephrine bitartrate/|Vasoconstrictor active ingredients. The active ingredient of the product consists of any of the following when used in the concentration or within the concentration range established for each ingredient. Phenylephrine hydrochloride 0.25 percent.|Ophthalmic vasoconstrictors. The active ingredient of the product consists of one of the following, within the established concentration for each ingredient. Phenylephrine hydrochloride, 0.08 to 0.2 percent.

DHHS/NTP; Toxicology & Carcinogenesis Studies of Phenylephrine Hydrochloride in F344/N Rats and B6C3F1 Mice (Feed Studies) Technical Report Series No. 322 (1987) NIH Publication No. 87-2578

|Warning|H302 (100%): Harmful if swallowed [Warning Acute toxicity, oral]|P264, P270, P301+P312, P330, and P501|Aggregated GHS information provided by 91 companies from 3 notifications to the ECHA C&L Inventory.|Danger|P261, P264, P270, P271, P272, P280, P285, P301+P312, P302+P352, P304+P312, P304+P340, P304+P341, P305+P351+P338, P312, P321, P322, P330, P333+P313, P337+P313, P342+P311, P363, P403+P233, P405, and P501|Aggregated GHS information provided by 2 companies from 1 notifications to the ECHA C&L Inventory. Each notification may be associated with multiple companies.

Patients experiencing and overdose may present with headache, hypertension, reflex bradycardia, tingling limbs, cardiac arrhythmias, and a feeling of fullness in the head. Overdose may be treated by supportive care and discontinuing phenylephrine, chronotropic medications, and vasodilators. Subcutaneous phentolamine may be used to treat tissue extravasation.

Administration of a 10% solution of phenylephrine hydrochloride to patients pretreated with 2% pilocarpine hydrochloride produces mydriasis but to a lesser degree than occurs in patients who are not receiving the miotic. Pilocarpine may prevent or reduce visual disturbances and the risk of increased intraocular pressure associated with mydriasis in some patients and may be used to hasten recovery from mydriasis after ophthalmologic examination. Phenylephrine may reduce ciliary and conjunctival congestion and accommodative myopia often encountered when miotics are used alone in the treatment of glaucoma, without compromising the effectiveness of glaucoma therapy.|Concomitant administration of phenylephrine with cycloplegic antimuscarinic drugs such as atropine sulfate, cyclopentolate hydrochloride, homatropine hydrobromide, or scopolamine hydrobromide produces increased dilation of the pupil which is of clinical value.|The possibility that digitalis can sensitize the myocardium to the effects of sympathomimetic drugs should be considered.|The cardiac and pressor effects of phenylephrine are potentiated by prior administration of monoamine oxidase (MAO) inhibitors because the metabolism of phenylephrine is reduced. The potentiation is greater following oral administration of phenylephrine than after parenteral administration of the drug because reduction of the metabolism of phenylephrine in the intestine results in increased absorption of the drug. Oral administration of phenylephrine to patients receiving a MAO inhibitor should be avoided. Parenteral administration of phenylephrine to these patients, if unavoidable, should be undertaken with extreme caution and initial doses should be small. Patients should consult a clinician before initiating anorectal phenylephrine therapy if they are receiving an MAO inhibitor.|For more Interactions (Complete) data for PHENYLEPHRINE (12 total), please visit the HSDB record page.

Carcinogenesis studies of USP grade phenylephrine hydrochloride were conducted by administering diets containing the chemical (99% pure) to F344/N rats and B6C3F1 mice of each sex ... for 2 yr. ... Doses of 0, 620, and 1,250 ppm for rats and 0, 1,250, and 2,500 ppm for mice. ... In the 2 yr studies, the approx amount of /cmpd/ consumed per day was 24 mg/kg for low dose rats, 50 mg/kg for high dose rats, 133 mg/kg for low dose mice, and 270 mg/kg for high dose mice. ... Under the conditions of these 2 yr studies, there was no evidence of carcinogenicity of phenylephrine hydrochloride for male or female F344/N rats given 620 or 1,250 ppm in feed or for male or female B6C3F1 mice given 1,250 or 2,500 ppm in feed. ... /Phenylephrine hydrochloride/|Phenylephrine hydrochloride was not mutagenic in four strains of Salmonella typhimurium (TA100, TA1535, TA1537, and TA98) with or without Aroclor 1254-induced liver S9 from male Sprague-Dawley rats or male Syrian hamsters. The results of mutagenicity studies of phenylephrine hydrochloride were equivocal in the mouse lymphoma L5178Y/TK+/- assay in the absence of S9; it was not tested in the presence of S9. Phenylephrine hydrochloride induced sister-chromatid exchanges (SCEs) but not chromosomal aberrations in Chinese hamster ovary cells. The increase in SCEs was seen only in the absence of metabolic activation with S9.

Phenylephrine generally is contraindicated for ophthalmic use in patients with angle-closure glaucoma and is contraindicated in those with known hypersensitivity to phenylephrine or other components of the commercially available solutions or in those with aneurysm.|The drug should be used with caution in patients with marked hypertension, cardiac disorders, advanced arteriosclerotic changes, type 1 (insulin-dependent, IDDM) diabetes mellitus, or hyperthyroidism; in children of low body weight; and in geriatric patients.|Unless otherwise directed by a clinician, patients should not receive external or rectal preparations of vasoconstrictors such as phenylephrine hydrochloride for self-medication of hemorrhoidal symptoms if they have cardiac disease, high blood pressure, thyroid disease, diabetes mellitus, or difficulty in urination secondary to prostatic hyperplasia. /Phenylephrine hydrochloride/|The drug should be administered with extreme caution to geriatric or hyperthyroid patients or those with bradycardia, partial heart block, myocardial disease, or severe arteriosclerosis. Some clinicians, however, consider severe coronary disease or cardiovascular disease (including myocardial infarction) to be contraindications to use of phenylephrine. Phenylephrine should be administered parenterally with extreme caution if at all to hypertensive patients. Phenylephrine is contraindicated in patients with severe hypertension or ventricular tachycardia and in patients who are hypersensitive to the drug. If administered to patients with acute pancreatitis or hepatitis, the drug may increase ischemia in the liver or pancreas. Phenylephrine should not be used in patients with peripheral or mesenteric vascular thrombosis, because ischemia may be increased and the area of infarction extended.

Data regarding the protein binding of phenylephrine in serum is not readily available.

Phenylephrine injections are indicated to treat hypotension caused by shock or anesthesia, an ophthalmic formulation is indicated to dilate pupils and induce vasoconstriction, an intranasal formulation is used to treat congestion, and a topical formulation is used to treat hemorrhoids. Off-label uses include situations that require local blood flow restriction such as the treatment of priapism.|Omidria is indicated in adults for maintenance of intraoperative mydriasis, prevention of intraoperative miosis and reduction of acute postoperative ocular pain in intraocular lens replacement surgery.

Adrenergic alpha-Agonists; Cardiotonic Agents; Mydriatics; Nasal Decongestants; Sympathomimetics; Vasoconstrictor Agents|Nasal phenylephrine is indicated for the symptomatic relief of nasal congestion due to the common cold or hay fever, sinusitis, or other upper respiratory allergies. /Included in US product labeling/|Nasal phenylephrine may be useful in the adjunctive therapy of middle ear infections by decreasing congestion around the eustachian ostia. /Included in US product labeling/|Nasal phenylephrine is used for relief of sinus congestion. /NOT included in US product labeling/|For more Therapeutic Uses (Complete) data for PHENYLEPHRINE (18 total), please visit the HSDB record page.

Because it is not known whether phenylephrine is distributed into milk, the drug should be used with caution in nursing women.|Administration of phenylephrine to patients in late pregnancy or labor may cause fetal anoxia and bradycardia by increasing contractility of the uterus and decreasing uterine blood flow. ... It is also not known whether the drug can cause fetal harm when administered to pregnant women. Phenylephrine should be used during pregnancy only when clearly needed.|Ophthalmic use of phenylephrine occasionally causes systemic sympathomimetic effects such as palpitation, tachycardia, premature ventricular contractions, occipital headache, pallor or blanching, trembling or tremors, increased perspiration, and hypertension. In one patient, hypertension severe enough to cause subarachnoid hemorrhage followed insertion of a cotton wick saturated with 10% phenylephrine hydrochloride in the lower conjunctival cul-de-sac. ... Systemic effects occur only rarely after topical application of solutions containing 2.5% or less of phenylephrine hydrochloride to the conjunctiva but are more likely to occur if the drug is instilled after the corneal epithelium has been damaged (e.g., by trauma or instrumentation) or permeability is increased by tonometry, inflammation, surgery of the eye or adnexa, or topical application of a local anesthetic; when the eye or adnexa are diseased; or when lacrimation is suppressed such as during anesthesia. The risk of severe hypertension is greatest in infants receiving instillations of 10% phenylephrine hydrochloride solutions.|In patients with shock, pressor therapy is not a substitute for replacement of blood, plasma, fluids, and/or electrolytes. Blood volume depletion should be corrected as fully as possible before phenylephrine is administered. In an emergency, the drug may be used as an adjunct to fluid volume replacement or as a temporary supportive measure to maintain coronary and cerebral artery perfusion until volume replacement therapy can be completed, but phenylephrine must not be used as sole therapy in hypovolemic patients. Additional volume replacement also may be required during or after therapy with the drug, especially if hypotension recurs. Monitoring of central venous pressure or left ventricular filling pressure may be helpful in detecting and treating hypovolemia; in addition, monitoring of central venous or pulmonary arterial diastolic pressure is necessary to avoid overloading the cardiovascular system and precipitating congestive heart failure. Hypoxia and acidosis, which also may reduce the effectiveness of phenylephrine, must be identified and corrected prior to or concurrently with administration of the drug.|For more Drug Warnings (Complete) data for PHENYLEPHRINE (24 total), please visit the HSDB record page.

Phenylephrine is an alpha-1 adrenergic agonist that raises blood pressure, dilates the pupils, and causes local vasoconstriction. Ophthalmic formulations of phenylephrine act for 3-8 hours while intravenous solutions have an effective half life of 5 minutes and an elimination half life of 2.5 hours. Patients taking ophthalmic formulations of phenylephrine should be counselled about the risk of arrhythmia, hypertension, and rebound miosis. Patients taking an intravenous formulation should be counselled regarding the risk of bradycardia, allergic reactions, extravasation causing necrosis or tissue sloughing, and the concomitant use of oxytocic drugs.

Compounds that bind to and activate ADRENERGIC ALPHA-1 RECEPTORS. (See all compounds classified as Adrenergic alpha-1 Receptor Agonists.)|Drugs that mimic the effects of stimulating postganglionic adrenergic sympathetic nerves. Included here are drugs that directly stimulate adrenergic receptors and drugs that act indirectly by provoking the release of adrenergic transmitters. (See all compounds classified as Sympathomimetics.)|Drugs used to cause constriction of the blood vessels. (See all compounds classified as Vasoconstrictor Agents.)|Agents that have a strengthening effect on the heart or that can increase cardiac output. They may be CARDIAC GLYCOSIDES; SYMPATHOMIMETICS; or other drugs. They are used after MYOCARDIAL INFARCT; CARDIAC SURGICAL PROCEDURES; in SHOCK; or in congestive heart failure (HEART FAILURE). (See all compounds classified as Cardiotonic Agents.)|Agents that dilate the pupil. They may be either sympathomimetics or parasympatholytics. (See all compounds classified as Mydriatics.)|Drugs designed to treat inflammation of the nasal passages, generally the result of an infection (more often than not the common cold) or an allergy related condition, e.g., hay fever. The inflammation involves swelling of the mucous membrane that lines the nasal passages and results in inordinate mucus production. The primary class of nasal decongestants are vasoconstrictor agents. (From PharmAssist, The Family Guide to Health and Medicine, 1993) (See all compounds classified as Nasal Decongestants.)

Phenylephrine is 38% orally bioavailable. Clinically significant systemic absorption of ophthalmic formulations is possible, especially at higher strengths and when the cornea is damaged.|86% of a dose of phenylephrine is recovered in the urine with 16% as the unmetabolized drug, 57% as the inactive meta-hydroxymendelic acid, and 8% as inactive sulfate conjugates.|The volume of distribution of phenylephrine is 340L.|Phenylephrine has an average clearance of 2100mL/min.|Phenylephrine undergoes rapid distribution into peripheral tissues; there is some evidence that the drug may be stored in certain organ compartments. The pharmacologic effects of phenylephrine are terminated at least partially by uptake of the drug into tissues. Penetration of phenylephrine into the brain appears to be minimal. Phenylephrine does not appear to be distributed to any great extent into breast milk.|Phenylephrine is completely absorbed following oral administration and undergoes extensive first-pass metabolism in the intestinal wall. The bioavailability of phenylephrine following oral administration is approximately 38% relative to IV administration. Because of extensive first-pass metabolism, there is considerable interindividual and possibly intraindividual variation in oral bioavailability of the drug. Following oral administration of phenylephrine (1 or 7.8 mg), peak serum concentrations occur at 0.75-2 hours.|Phenylephrine and its metabolites are excreted mainly in urine. Following oral or IV administration, approximately 80 or 86% of the dose, respectively, is excreted in urine within 48 hours, principally as metabolites; approximately 2.6% of an oral dose or 16% of an IV dose is excreted in urine as unchanged drug.|7-3H-phenylephrine was given to 15 volunteers by a short-infusion n = 4) or p.o. (10 volunteers, 1 patient with porto-caval anastomosis). Analysis of serum for free 3H-phenylephrine and fractionation of urinary radioactivity was performed by ion-exchange and thin-layer chromatography. As almost the same 3H-activity was excreted in urine after i.v. and p.o. administration, 86% and 80% of the dose respectively, complete enteral absorption can be assumed. A considerable difference was seen in the fraction of free phenylephrine, i.v. 16% of the dose versus p.o. 2.6%, which suggested reduced bioavailability. This was confirmed by comparison of the areas under the serum curve, which showed a bioavailability factor of 0.38. The result for the patient with porto-caval anastomosis was comparable to that in the normal volunteers. The biological half-life of 2 to 3hr was comparable to that of structurally related amines, as were the total clearance of 2 L/hr, and the volume of distribution of 340 L.

Phenylephrine is mainly metabolized by monoamine oxidase A, monoamine oxidase B, and SULT1A3. The major metabolite is the inactive meta-hydroxymandelic acid, followed by sulfate conjugates. Phenylephrine can also be metabolized to phenylephrine glucuronide.|Phenylephrine undergoes extensive metabolism in the intestinal wall (first-pass) and in the liver. The principal routes of metabolism involve sulfate conjugation (primarily in the intestinal wall) and oxidative deamination (by monoamine oxidase (MAO)); glucuronidation also occurs to a lesser extent.|7-3H-phenylephrine was given to 15 volunteers by a short-infusion n = 4) or p.o. (10 volunteers, 1 patient with porto-caval anastomosis). Analysis of serum for free 3H-phenylephrine and fractionation of urinary radioactivity was performed by ion-exchange and thin-layer chromatography. ... Metabolism to phenolic conjugates mainly after oral ingestion, and to m-hydroxymandelic acid after i.v. injection, again demonstrated that m-hydroxylated amines are predominantly conjugated during the "first-pass" metabolism.|Phenylephrine has known human metabolites that include (2S,3S,4S,5R)-3,4,5-trihydroxy-6-[3-[(1R)-1-hydroxy-2-(methylamino)ethyl]phenoxy]oxane-2-carboxylic acid.

Intravenous phenylephrine has an effective half life of 5 minutes and an elimination half life of 2.5 hours.|The elimination half-life of phenylephrine averages 2-3 hours following oral or IV administration

Phenylephrine is an alpha-1 adrenergic agonist that mediates vasoconstriction and mydriasis depending on the route and location of administration. Systemic exposure to phenylephrine also leads to agonism of alpha-1 adrenergic receptors, raising systolic and diastolic pressure as well as peripheral vascular resistance. Increased blood pressure stimulates the vagus nerve, causing reflex bradycardia.|Phenylephrine acts predominantly by a direct effect on alpha-adrenergic receptors. In therapeutic doses, the drug has no substantial stimulant effect on the beta-adrenergic receptors of the heart (beta1-adrenergic receptors) but substantial activation of these receptors may occur when larger doses are given. Phenylephrine does not stimulate beta-adrenergic receptors of the bronchi or peripheral blood vessels (beta2-adrenergic receptors). It is believed that alpha-adrenergic effects result from the inhibition of the production of cyclic adenosine-3',5'-monophosphate (cAMP) by inhibition of the enzyme adenyl cyclase, whereas beta-adrenergic effects result from stimulation of adenyl cyclase activity. Phenylephrine also has an indirect effect by releasing norepinephrine from its storage sites.

Emergency and Supportive Measures: Maintain an open airway and assist ventilation if necessary. Administer supplemental oxygen. Treat hypertension aggressively. Treat seizures and ventricular tachyarrhythmias if they occur. Do not treat reflex bradycardia except indirectly by lowering blood pressure. Monitor the vital signs and ECG for a minimum of 4-6 hours after exposure and longer if a sustained-release preparation has been ingested. /Pseudoephedrine, phenylephrine, and other decongestants/|Specific Drugs and Antidotes: Hypertension. Treat hypertension if the diastolic pressure is higher than 100-105 mm Hg, especially in a patient with no prior history of hypertension. If there is CT or obvious clinical evidence of intracranial hemorrhage, lower the diastolic pressure cautiously to no lower than 90 mm Hg and consult a neurosurgeon immediately. Use a vasodilator such as phentolamine or nitroprusside. Caution: Do not use beta blockers to treat hypertension without first giving a vasodilator; otherwise, paradoxic worsening of the hypertension may result. Many patients have moderate orthostatic variation in blood pressure; therefore, for immediate partial relief of severe hypertensin, try placing the patient in an upright position. Arrhythmias. Tachyarrhythmias usually respond to low-dose esmolol for metoprolol. Caution: Do not treaT AV block or sinus bradycardia associated with hypertension; increasing the heart rate with atropine may abolish this reflex response that serves to limit hypertension, resulting in worsening elevation of the blood pressure. /Pseudoephedrine, phenylephrine, and other decongestants/|Decontamination. Administer activated charcoal orally if conditions are appropriate. Gastric lavage is not necessary after small to moderate ingestions if activated charcoal can be given promptly. /Pseudoephedrine, phenylephrine, and other decongestants/|Enhanced Elimination. Dialysis and hemoperfusion are not effective. Urinary acidification may enhance elimination of phenylpropanolamine, ephedrine, and pseudoephedrine but may also aggravate myoglobin deposition in the kidney if the patient has rhabdomyolysis. /Pseudoephedrine, phenylephrine, and other decongestants/

/SIGNS AND SYMPTOMS/ Overdosage of phenylephrine may cause hypertension, headache, seizures, cerebral hemorrhage, palpitation, paresthesia, or vomiting. Headache may be a symptom of hypertension. Hypertension may be relieved by administration of an alpha-adrenergic blocking agent (e.g., phentolamine). If phenylephrine is administered by rapid IV injection ... overdosage may result in short paroxysms of ventricular tachycardia, ventricular extrasystoles, or a sensation of fullness in the head.|/SIGNS AND SYMPTOMS/ Severe and sometimes fatal cardiovascular reactions, including ventricular arrhythmias and myocardial infarction, have occurred rarely following topical application of 10% phenylephrine hydrochloride ophthalmic solutions; these reactions have occurred most frequently in geriatric patients with preexisting cardiovascular disease.|/CASE REPORTS/ A 71-year-old woman who had critical cerebral ischemia secondary to a carotid artery occlusion was receiving high-dose intravenous phenylephrine for a trial of hypertensive therapy. While on a maximal dose of phenylephrine she developed prominent positive U waves, which disappeared with the cessation of the drug.|/CASE REPORTS/ Four patients (age range 54-82, 1F 3M) diagnosed with non-arteritic ischemic optic neuropathy experienced acute worsening of visual function after instillation of phenylephrine for dilated funduscopic examination. They experienced decreased visual function immediately or shortly after administration of topical mydriatic drops given in preparation for funduscopy. In all cases one drop each of 2.5% phenylephrine and 0.5-1% tropicamide was used. Three patients had classical risk factors such as hypertension, diabetes, and had a contralateral "disc-at-risk". The female and youngest patient had ischemic optic neuropathy presumed secondary to lupus erythematosus. The time from acute visual loss to presentation to neuro-ophthalmic care ranged from 1-6 days. The time of onset of the decline in visual function varied from 45 minutes (patient with lupus) to 12 hours after instillation of mydriatic drops. Visual acuity at diagnosis ranged from 20/40-20/400. Phenylephrine is a mydriatic with vasoconstrictive properties, which may be absorbed through the cornea, thus yielding non-negligible intraocular concentrations. Vasoconstriction of the watershed posterior ciliary capillary beds may result in further precipitating infarction of already compromised circulatory territories in edematous optic nerves. Because phenylephrine is a known vasoconstrictor in vivo and in vitro, it is more likely to cause deleterious vasoconstriction and an acute decline in visual function in patients with acute ischemic optic neuropathy than tropicamide. ...|For more Human Toxicity Excerpts (Complete) data for PHENYLEPHRINE (11 total), please visit the HSDB record page.

(R)-3-Hydroxy-alpha-((methylamino)methyl)benzenemethanol

Oral: Strips, orally dissolving: 1.25 mg Triaminic Infant Thin Strips Decongestant, (Novartis) 2.5 mg Triaminic Thin Strips Cold, (Novartis). Tablets: 10 mg Sudafed PE, (Pfizer). Parenteral: Injection: 10 mg/mL Neo-Synephrine Hydrochloride (with sodium metabisulfite), (Sanofi-Aventis), Phenylephrine Hydrochloride Injection, (American Regent), Phenylephrine Hydrochloride Injection, (Baxter). Topical: Cream: 0.25% with Glycerin 12%, (Petrolatum); 18%, and Shark Liver Oil 3% Preparation H (with cetyl alcohol, methylparaben, and stearyl alcohol), (Wyeth). Gel: 0.25% with Witch Hazel 50% Preparation H (with methylparaben and propylparaben), (Wyeth). Ointment: 0.25% with Mineral Oil 14%, Petrolatum 71.9%, and Shark Liver Oil 3% Preparation H (with methylparaben and propylparaben), (Wyeth). Suppository: 0.25% with Cocoa Butter 85.5% and Shark Liver Oil 3% Preparation H (with methylparaben and propylparaben), (Wyeth).|Nasal: Solution: 0.25% Neo-Synephrine Mild Formula Spray (with benzalkonium chloride), (Bayer); 0.5% Neo-Synephrine Regular Strength (with benzalkonium chloride; drops and spray), (Bayer), Vicks Sinex for Sinus Relief (with benzalkonium chloride; regular or metered pump mist spray), (Procter & Gamble); 1% Neo-Synephrine Extra Strength (with benzalkonium chloride; drops and spray), (Bayer). Ophthalmic: Solution: 0.12% Ocu-Phrin, Ocumed Relief (with benzalkonium chloride), (Allergan); 2.5% AK-Dilate (with benzalkonium chloride and sodium bisulfite), (Akorn), Mydfrin (with benzalkonium chloride and sodium bisulfite), (Alcon) Neo-Synephrine Hydrochloride (with benzalkonium chloride), (Sanofi-Aventis), Ocu-Phrin, (Ocumed); 10% AK-Dilate (with benzalkonium chloride and sodium bisulfite), (Akorn), Neo-Synephrine Hydrochloride (with benzalkonium chloride; plain and viscous), (Sanofi-Aventis), Ocu-Phrin, (Ocumed). Parenteral: Injection: 10 mg/mL Neo-Synephrine Hydrochloride (with sodium metabisulfite), (Sanofi-Aventis), Phenylephrine Hydrochloride Injection, (American Regent), Phenylephrine Hydrochloride Injection, (Baxter). /Phenylephrine hydrochloride/|Ophthalmic: Solution: 0.12% Ocu-Phrin, (Ocumed), Relief (with benzalkonium chloride; viscous), (Allergan); 2.5% AK-Dilate (with benzalkonium chloride and sodium bisulfite), (Akorn), Mydfrin (with benzalkonium chloride and sodium bisulfite), (Alcon), Neo-Synephrine Hydrochloride (with benzalkonium chloride), (Sanofi-Aventis), Ocu-Phrin, (Ocumed), Phenylephrine Hydrochloride Ophthalmic Solution, (Bausch & Lomb), Phenylephrine Hydrochloride Ophthalmic Solution, (Falcon); 10% AK-Dilate (with benzalkonium chloride and sodium bisulfite), (Akorn), Neo-Synephrine Hydrochloride (with benzalkonium chloride; plain and viscous), (Sanofi-Aventis), Ocu-Phrin, (Ocumed). /Phenylephrine hydrochloride/

THIN LAYER CHROMATOGRAPHY AND GAS LIQUID CHROMATOGRAPHY.|38.180-38.193. 38.180: ULTRAVIOLET SPECTROPHOTOMETRY; 38.181-38.183: COLORIMETRY; 38.184- 38.193: AUTOMATED METHOD /PHENYLEPHRINE HYDROGEN CHLORIDE/|HIGH PERFORMANCE LIQUID CHROMATOGRAPHY IN PARTIAL ELECTROLYSIS ELECTROCHEMICAL DETECTOR.

URINE-BLOOD, FLUOROMETRY, EXCITATION 525 NM/EMISSION 570 NM.|DETERMINATION IN URINE USING GAS CHROMATOGRAPHY.

Human drugs -> Omidria -> EMA Drug Category|Ophthalmologicals -> Human pharmacotherapeutic group|Human Drugs -> FDA Approved Drug Products with Therapeutic Equivalence Evaluations (Orange Book) -> Active Ingredients