L-Norephedrin

0.67

log Kow = 0.67

Freely soluble

Freely soluble in water and alcohol

190-194 °C

101-101.5 °C

Solid. Mol wt: 187.69, mp: 194 °C. Soluble in water. /Hydrochloride/

9.44 (at 20 °C)

pKa = 9.44 (conjugate acid)

1313；1304；1308；1308；1287；1300；1291；1310；1310；1302.6；1287；1304；1308；1310；1313

1289；1321；1326；1331；1331；1332；1339

2231

Crystals; melting point 190-194 °C; odor resembling that of crude benzoic acid; pKa 9.44 + or - 0.04. Freely soluble in water, alcohol; practically insoluble in ether, chloroform, benzene. The aq soln is neutral to litmus. /Phenylpropanolamine hydrochloride/

Melting point: 171-172 °C; Specific optical rotation: +32 deg at 25 °C/D (Water) /(+)-Form hydrochloride/

Warning

H302 (100%): Harmful if swallowed [Warning Acute toxicity, oral]；H315 (100%): Causes skin irritation [Warning Skin corrosion/irritation]；H319 (100%): Causes serious eye irritation [Warning Serious eye damage/eye irritation]；H335 (100%): May cause respiratory irritation [Warning Specific target organ toxicity, single exposure; Respiratory tract irritation]

P261, P264, P264+P265, P270, P271, P280, P301+P317, P302+P352, P304+P340, P305+P351+P338, P319, P321, P330, P332+P317, P337+P317, P362+P364, P403+P233, P405, and P501 (click each P-code to see the statement)

Aggregated GHS information provided per 41 reports by companies from 3 notifications to the ECHA C&L Inventory. Each notification may be associated with multiple companies.；Information may vary between notifications depending on impurities, additives, and other factors. The percentage value in parenthesis indicates the notified classification ratio from companies that provide hazard codes. Only hazard codes with percentage values above 10% are shown. For more detailed information, please visit ECHA C&L website.

List I Chemical: A chemical specified by regulation that, in addition to legitimate uses, is used in manufacturing a controlled substance in violation of the Act and is important to the manufacture of a controlled substance. (21 eCFR 1310.02)

Status: Active Update: 22-06-2020 https://echa.europa.eu/registration-dossier/-/registered-dossier/23968

Phenylpropanolamine: Does not have an individual approval but may be used as a component in a product covered by a group standard. It is not approved for use as a chemical in its own right.

The Approved Drug Products with Therapeutic Equivalence Evaluations List identifies discontinued drug products. Phenylpropanolamine hydrochloride is included on this list. /Phenylpropanolamine Hydrochloride/

The Approved Drug Products with Therapeutic Equivalence Evaluations List identifies discontinued drug products. Phenylpropanolamine polistirex is included on this list. /Phenylpropanolamine Polistirex /

The Food and Drug Administration (FDA) is issuing a public health advisory concerning phenylpropanolamine hydrochloride. This drug is widely used as a nasal decongestant (in over-the-counter and prescription drug products) and for weight control (in over-the-counter drug products). FDA is taking steps to remove phenylpropanolamine from all drug products and has requested that all drug companies discontinue marketing products containing phenylpropanolamine. Phenylpropanolamine has been marketed for many years. A recent study reported that taking phenylpropanolamine increases the risk of hemorrhagic stroke (bleeding into the brain or into tissue surrounding the brain) in women. Men may also be at risk. Although the risk of hemorrhagic stroke is very low, FDA recommends that consumers not use any products that contain phenylpropanolamine.

Wellman PJ; The Pharmacology of the Anorexic Effect of Phenylpropanolamine; Drugs Exp Clin Res 16 (9): 487-95 (1990).

Lake CR et al; Adverse Drug Effects Attributed to Phenylpropanolamine: A Review of 142 Case Reports; Am J Med 89 (2): 195-208 (1990).

Forman HP et al; Cerebral Vasculitis and Hemorrhage in an Adolescent Taking Diet Pills Containing Phenylpropanolamine: Case Report and Review of Literature; Pediatrics 83 (5): 737-41 (1989). In this report, the 11th documented case of phenylpropanolamine-associated intracerebral hemorrhage with vasculitis is described. This is the first case in an adolescent following the ingestion of an overdose of diet aid pills.

Dilsaver SC et al; Complications of Phenylpropanolamine; Am Fam Physician 39 (4): 201-6 (1989).

For more Special Reports (Complete) data for PHENYLPROPANOLAMINE (9 total), please visit the HSDB record page.

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.

With amphetamines, phenylpropanolamine, and the tricyclic antidepressants, the antihypertensive effects of methyldopa are lessened.

Concomitant use /of/ phenylpropanolamine and indomethacin was associated with severe hypertension in one patient; hypertension did not occur when either drug was used alone. /Phenylpropanolamine hydrochloride/

Administration of phenylpropanolamine to patients who have received cyclopropane or halogenated hydrocarbon general anesthetics may result in arrhythmias. Arrhythmias, if they occur, may respond to administration of propranolol, a beta-adrenergic blocking agent. /Phenylpropanolamine hydrochloride/

The effects of caffeine and phenylpropanolamine are mediated through activation of the central and sympathetic nervous systems. Severe, life threatening, and occasionally fatal hypertensive reactions have been reported after their combined use. This study examined the possible pharmacokinetic interaction of phenylpropanolamine and caffeine. Sixteen normal subjects received combinations of caffeine, phenylpropanolamine, and placebo. In subjects receiving 400 mg caffeine plus 75 mg phenylpropanolamine, the mean (+ or - SEM) peak plasma caffeine concentration of 8.0 + or - 2.2 ug/mL was significantly greater than after 400 mg caffeine alone (2.1 + or - 0.3 ug/mL; t(24) = 2.4; p < 0.01). Physical side effects were more frequent after the phenylpropanolamine-caffeine combination than after either drug alone or after placebo. Greater increases in both systolic and diastolic blood pressures occurred after the combination than after either drug alone. These data indicate that phenylpropanolamine may enhance absorption or inhibit elimination of caffeine and may explain increased side effects reported after their combined use.

For more Interactions (Complete) data for PHENYLPROPANOLAMINE (15 total), please visit the HSDB record page.

TERRESTRIAL FATE: Based on a classification scheme(1), an estimated Koc value of 55(SRC), determined from a log Kow of 0.67(2) and a regression-derived equation(3), indicates that phenylpropanolamine is expected to have high mobility in soil(SRC). The pKa of phenylpropanolamine is 9.44(4), indicating that this compound will primarily exist in cation form and cations generally adsorb more strongly to soils containing organic carbon and clay than their neutral counterparts(5). Phenylpropanolamine is not expected to volatilize from dry soil surfaces(SRC) based upon an estimated vapor pressure of 8.7X10-4 mm Hg(SRC), determined from a fragment constant method(6). Phenylpropanolamine has been categorized as a compound that is readily biodegradable after acclimatization(7).

AQUATIC FATE: Based on a classification scheme(1), an estimated Koc value of 55(SRC), determined from a log Kow of 0.67(2) and a regression-derived equation(3), indicates that phenylpropanolamine is not expected to adsorb to suspended solids and sediment(SRC). A pKa of 9.44(4) indicates phenylpropanolamine will primarily exist in the cation form at pH values of 5 to 9 and therefore volatilization from water surfaces is not expected to be an important fate process(5). According to a classification scheme(6), an estimated BCF of 3(SRC), from its log Kow(2) and a regression-derived equation(7), suggests the potential for bioconcentration in aquatic organisms is low(SRC). Phenylpropanolamine has been categorized as a compound that is readily biodegradable after acclimatization(8).

ATMOSPHERIC FATE: According to a model of gas/particle partitioning of semivolatile organic compounds in the atmosphere(1), phenylpropanolamine, which has an estimated vapor pressure of 8.7X10-4 mm Hg at 25 °C(2), is expected will exist in both the vapor and particulate phases in the ambient atmosphere. Vapor-phase phenylpropanolamine is degraded in the atmosphere by reaction with photochemically-produced hydroxyl radicals(SRC); the half-life for this reaction in air is estimated to be 7 hours(SRC), calculated from its estimated rate constant of 5.7X10-11 cu cm/molecule-sec at 25 °C(3). Particulate-phase phenylpropanolamine may be removed from the air by wet or dry deposition(SRC). Phenylpropanolamine does not contains chromophores that absorb at wavelengths >290 nm and therefore is not expected to be susceptible to direct photolysis by sunlight(4).

The Koc of phenylpropanolamine is estimated as 55(SRC), using a log Kow of 0.67(1) and a regression-derived equation(2). According to a classification scheme(3), this estimated Koc value suggests that phenylpropanolamine is expected to have high mobility in soil. The pKa of phenylpropanolamine is 9.94(4), indicating that this compound will primarily exist in the cation form in the environment and cations generally adsorb more strongly to soils containing organic carbon and clay than their neutral counterparts(5).

/HUMAN EXPOSURE STUDIES/ Based upon 726 first trimester exposures, a possible association was found with malformations including: hypospadias, eye and ear defects, polydactyly, cataracts and pectus excavatum. After 2489 exposures during anytime of pregnancy, 12 infants had congenital dislocation of the hip. /From table/

/SIGNS AND SYMPTOMS/ The acute effects of a single capsule of each of two phenylpropanolamine-containing preparations were determined in a group of healthy young adults, by means of a double-blind comparison with matching placebo preparations. Supine diastolic blood-pressure rose to 100 mm Hg or more in 12 out of 37 subjects taking an anorectic preparation ( ... 85 mg phenylpropanolamine per capsule) and in 4 out of 34 subjects taking a decongestant preparation ( ... 50 mg phenylpropanolamine per capsule). Twenty of the subjects taking ... /the 85 mg capsules/ reported adverse side effects. The frequency and extent of the hypertensive response to high-dose phenylpropranolamine-containing preparations suggest that clinical use of such preparations should be reviewed and that their availability without prescription may not be appropriate.

/SIGNS AND SYMPTOMS/ The variability in pharmacokinetic parameters and the relationship between phenylpropanolamine blood concentrations and blood pressure response were studied in 10 normal volunteers (mean age, 27.1 yr) following an intravenous injection of 0.44 mg/kg phenylpropanolamine hydrochloride. Mean blood pressure increased by 24/16 mm Hg after phenylpropanolamine and was statistically significant compared with placebo response. Injection of phenylpropanolamine was terminated in 2 volunteers due to excessive increases in blood pressure. The hyperresponders had the lowest peak phenylpropanolamine serum concentrations. A pharmacokinetic basis for the variability in response to phenylpropanolamine was not observed. A relationship did not exist within the group between blood pressure effect and serum concentration but did exist within each subject. It was concluded that the blood pressure effect of phenylpropanolamine in an individual cannot be predicted solely from serum concentration. /Phenylpropanolamine Hydrochloride/

/SIGNS AND SYMPTOMS/ ... SOPHIA (the study of pulmonary hypertension in America), in addition to confirming previous reports of a causal association between the appetite suppressant fenfluramine and pulmonary arterial hypertension, unexpectedly found a significantly increased risk for the development of pulmonary arterial hypertension with exposure to over-the-counter antiobesity agents containing phenylpropanolamine. The first case is reported of fatal pulmonary arterial hypertension in a child heavily treated with cold remedies containing phenylpropanolamine, which, in addition to the results of SOPHIA, strengthens the hypothesis that phenylpropanolamine is a risk factor for the development of pulmonary arterial hypertension.

For more Human Toxicity Excerpts (Complete) data for PHENYLPROPANOLAMINE (21 total), please visit the HSDB record page.

Phenylpropanolamine's production and use as the hydrochloride which is used as an anorexic and as a decongestant and in the treatment of urinary incontinence in humans, cats, and dogs(1) may result in its release to the environment through various waste streams(SRC).

An estimated BCF of 3 was calculated in fish for phenylpropanolamine(SRC), using a log Kow of 0.67(1) and a regression-derived equation(2). According to a classification scheme(3), this BCF suggests the potential for bioconcentration in aquatic organisms is low(SRC).

Phenylpropanolamine's pKa of 9.44(1) indicates that volatilization from moist soil surfaces may not occur(SRC) as cations to adsorb more strongly to soils than their neutral counterparts(2). Phenylpropanolamine is not expected to volatilize from dry soil surfaces(SRC) based upon an estimated vapor pressure of 8.7X10-4 mm Hg(SRC), determined from a fragment constant method(3).

/LABORATORY ANIMALS: Acute Exposure/ Overdose with the sympathomimetic agent phenylpropanolamine may cause arrhythmias and myocardial injury in humans. To study the mechanism of these toxic effects, unanesthetized rats (6 animals per group) were given single intraperitoneal doses of 1, 2, 4, 8, 16, or 32 mg/kg phenylpropanolamine. Increases in blood pressure, measured by tail cuff, were dose related and comparable to increases reported in patients with phenylpropanolamine toxicity. Animals were killed at 24 hr and light microscopic examination showed diffuse, dose related myocardial necrosis. Histology scores (a measure of severity of necrosis) in groups receiving 8, 16, and 32 mg/kg phenylpropanolamine were 1.4 + or - 0.5, 1.8 + or - 1.0, and 2.3 + or - 0.4, respectively, and were all significantly greater than the histology score of control animals (0.2 + or - 0.3, p < 0.01). The observed lesion was similar in appearance to the myocardial necrosis produced by large doses of catecholamines or sympathomimetic agents in rats. In summary, single doses of phenylpropanolamine caused myocardial necrosis in rats at doses comparable to those causing toxicity in humans. Myocardial necrosis may contribute to the cardiac toxicity of phenylpropanolamine overdose.[Pentel PR et al; Fundam Appl Toxicol 9 (1): 167-72 (1987)]

/LABORATORY ANIMALS: Neurotoxicity/ For decades, the sympathomimetic phenylpropanolamine (PPA; +/--norepinephrine) was an active ingredient found in popular children's over-the-counter (OTC) cold, cough, and allergy medications. To examine the possibility that pre-adolescent PPA exposure may induce neuroadaptations that influence behavioral and neurochemical responding to cocaine, C57BL/6J mice were pretreated with PPA (0-40 mg/kg) during postnatal days 21-31. The behavioral and neurochemical responses to acute and repeated cocaine (4 x 15 mg/kg) were then assessed in adulthood when the mice were 10 weeks of age. Whereas pre-adolescent PPA exposure did not influence the acute locomotor response to 15 mg/kg cocaine, PPA pre-exposure dose-dependently enhanced the expression of cocaine-induced place conditioning, reduced the expression of locomotor sensitization, but did not influence cocaine-induced stereotypy. Pre-adolescent PPA exposure completely prevented the capacity of cocaine to elevate extracellular levels of catecholamines in the nucleus accumbens, but facilitated the development of cocaine-induced glutamate sensitization. Neither acute nor repeated cocaine altered extracellular GABA levels in the accumbens of control mice; however, 15 mg/kg cocaine lowered GABA levels by approximately 40% in PPA pretreated mice and this effect showed tolerance with repeated cocaine administration. These data provide the first evidence that early exposure to an OTC compound produces protracted effects upon cocaine-induced changes in nucleus accumbens neurotransmission ... .[Szumlinski KK et al; Neuropsychopharmacology Jan 24 (Epub ahead of print) (2007)]

/OTHER TOXICITY INFORMATION/ A 5-year-old, 29-kg, female Labrador retriever developed tachypnea, tachycardia, and ataxia following ingestion of approximately 48 mg/kg of phenylpropanolamine. Initial diagnostic tests showed multiform ventricular tachycardia, left ventricular dilatation with a focal dyskinetic region in the dorsal interventricular septum, and elevations in creatinine kinase and cardiac troponin I. All abnormalities resolved within 6 months. The transient electrocardiographic, echocardiographic, and biochemical abnormalities were consistent with myocardial necrosis from infarction or direct catecholamine-induced myocardial toxicity.[Crandell JM et al; J of the American Animal Hospital Assn 41:413-20 (2005)]

... /The authors/ report a case of paranoid psychosis following use of a decongestant containing phenylpropanolamine and summarize the case report literature of psychiatric adverse effects to phenylpropanolamine in which doses were known and stated to be within recommended guidelines. A pattern of possible risk factors emerges from these reports. These may include 1) symptoms or history of mood spectrum disorder, 2) history of psychosis, 3) female sex, 4) family history of psychiatric disorder. ...

Phenylpropanolamine is contraindicated in patients with diabetes mellitus, heart disease, hyperthyroidism, and hypertension. Other contraindications include glaucoma, mental depression, MAOI use, hypersensitivity history, prostatic hypertrophy, and renal disease.

The rate constant for the vapor-phase reaction of phenylpropanolamine with photochemically-produced hydroxyl radicals has been estimated as 5.7X10-11 cu cm/molecule-sec at 25 °C(1). This corresponds to an atmospheric half-life of about 7 hours at an atmospheric concentration of 5X10+5 hydroxyl radicals per cu cm(1). Phenylpropanolamine is not expected to undergo hydrolysis in the environment due to the lack of functional groups that hydrolyze under environmental conditions(2). Phenylpropanolamine does not contain chromophores that absorb at wavelengths >290 nm and therefore is not expected to be susceptible to direct photolysis by sunlight(2).

NIOSH (NOES Survey 1981-1983) has statistically estimated that 934 workers (506 of these are female) are potentially exposed to phenylpropanolamine in the US(1). Phenylpropanolamine has been used in the medical industry for more than 30 years primarily as a nasal decongestant and an ingredient in cold remedies; it was the only FDA (1978) appetite suppressant as of 1985 that was sold without a prescription in the US(2). Occupational exposure to phenylpropanolamine may occur through dermal contact with this compound at workplaces where the hydrdochloride is produced or used(SRC). The general population may be exposed to phenylpropanolamine through ingestion and use of products containing this compound(SRC).

List I Chemical: A chemical specified by regulation that, in addition to legitimate uses, is used in manufacturing a controlled substance in violation of the Act and is important to the manufacture of a controlled substance. (21 eCFR 1310.02)

Status: Active Update: 22-06-2020 https://echa.europa.eu/registration-dossier/-/registered-dossier/23968

Phenylpropanolamine: Does not have an individual approval but may be used as a component in a product covered by a group standard. It is not approved for use as a chemical in its own right.

The Approved Drug Products with Therapeutic Equivalence Evaluations List identifies discontinued drug products. Phenylpropanolamine hydrochloride is included on this list. /Phenylpropanolamine Hydrochloride/

The Approved Drug Products with Therapeutic Equivalence Evaluations List identifies discontinued drug products. Phenylpropanolamine polistirex is included on this list. /Phenylpropanolamine Polistirex /

The Food and Drug Administration (FDA) is issuing a public health advisory concerning phenylpropanolamine hydrochloride. This drug is widely used as a nasal decongestant (in over-the-counter and prescription drug products) and for weight control (in over-the-counter drug products). FDA is taking steps to remove phenylpropanolamine from all drug products and has requested that all drug companies discontinue marketing products containing phenylpropanolamine. Phenylpropanolamine has been marketed for many years. A recent study reported that taking phenylpropanolamine increases the risk of hemorrhagic stroke (bleeding into the brain or into tissue surrounding the brain) in women. Men may also be at risk. Although the risk of hemorrhagic stroke is very low, FDA recommends that consumers not use any products that contain phenylpropanolamine.

R - Respiratory system；R01 - Nasal preparations；R01B - Nasal decongestants for systemic use；R01BA - Sympathomimetics；R01BA01 - Phenylpropanolamine

QR - Respiratory system；QR01 - Nasal preparations；QR01B - Nasal decongestants for systemic use；QR01BA - Sympathomimetics；QR01BA01 - Phenylpropanolamine

Phenylpropanolamine (PPA), a sympathomimetic agent structurally similar to pseudoephedrine, is used to treat nasal congestion. Phenylpropanolamine is found in appetite suppressant formulations and with guaifenesinin in cough-cold formulations. In 2000, the FDA requested that all drug companies discontinue marketing products containing phenylpropanolamine, due to an increased risk of hemorrhagic stroke in women who used phenylpropanolamine.

Phenylpropanolamine acts directly on alpha- and, to a lesser degree, beta-adrenergic receptors in the mucosa of the respiratory tract. Stimulation of alpha-adrenergic receptors produces vasoconstriction, reduces tissue hyperemia, edema, and nasal congestion, and increases nasal airway patency. PPA indirectly stimulates beta-receptors, producing tachycardia and a positive inotropic effect.

The mechanism of action of phenylpropanolamine has not been conclusively determined. The drug may directly stimulate adrenergic receptors but probably indirectly stimulates both A- and B-adrenergic receptors by releasing norepinephrine from its storage sites. It is believed that B-adrenergic effects result from stimulation of cyclic adenosine 3',5'-monophosphate (AMP) production by activation of the enzyme adenyl cyclase, whereas A-adrenergic effects result from inhibition of adenyl cyclase activity. With prolonged use or too frequent administration, indirectly acting sympathomimetics may deplete norepinephrine in sympathetic nerve endings and tachyphylaxis may develop. Tachyphylaxis induced by one indirectly acting sympathomimetic may result in refractoriness to other drugs of the same class. /Phenylpropanolamine hydrochloride/

Whether the alpha1- and alpha2-adrenoceptor mediated increases in diastolic blood pressure effected by phenylpropanolamine and its enantiomers are altered by, or independent of beta2-mediated vasodilation, or beta2-adrenoceptor blockade were studied in pithed rats. The pressor responses were enhanced in the presence of the antagonist ICI-118551 and diminished in the presence of albuterol. It was concluded that each form of phenylpropanolamine possesses the intrinsic ability to interact with all of the adrenoceptors in the system used and that the interaction with those adrenoceptors determines the net increase in diastolic blood pressure that follows the intravenous administration of the compounds. These findings have a bearing on the recent controversy regarding the use of beta-blocking agents in the treatment of overdosage of phenylpropanolamine.

2.1 to 3.4 hours.

The half-life ranges from 2.7 to 3.4 hrs. /Phenylpropanolamine hydrochloride/

Phenylpropanolamine reportedly has a half-life of 3-4 hours. /Phenylpropanolamine hydrochloride/

The bioavailability and pharmacokinetics of phenylpropanolamine hydrochloride (PPA HCl) from a controlled-release (CR) caplet and solution was studied in 12 male subjects, who received either a 75 mg PPA HCl CR caplet once daily or a 25 mg PPA HCl solution given three times a day. All subjects received the medication for 4 consecutive days. ... The mean elimination half-life for PPA HCl from the CR caplet was 5.84 hr and 3.73 hr, for the solution. ...

Hepatic

Like other phenylisopropanolamines, small amounts of the drug are slowly metabolized in the liver to an active hydroxylated metabolite. About 80-90% of a dose of phenylpropanolamine is excreted unchanged in the urine within 24 hours. /Phenylpropanolamine hydrochloride/

Drugs that selectively bind to and activate alpha adrenergic receptors.

Agents that are used to suppress appetite.

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.

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)

Reduced bioavailability (about 38%) from gastrointestinal tract because of first pass metabolism by monoamine oxidase in the stomach and liver.

Phenylpropanolamine is well absorbed orally, and the peak blood concentration is attained within one to two hours. ... The drug is principally excreted unchanged; the major route of excretion is renal. Since phenylpropanolamine is a weak base, elimination is enhanced in acid urine.

Phenylpropanolamine is readily absorbed from the GI tract. Nasal decongestion reportedly occurs within 15-30 minutes after oral administration of 25 mg of phenylpropanolamine hydrochloride and appears to persist for 3 hours. Plasma concentrations of the drug required for a therapeutic effect are not known. In one study, peak plasma concentrations of 100 ng/mL were reached in 1-2 hours and concentrations remained greater than 60 ng/ml for 6 hours following oral administration of 50 mg of phenylpropanolamine hydrochloride to fasting adults. Following administration of 150 mg of an extended-release preparation of the drug, peak plasma concentrations of 300 ng/mL occurred after 3.5 hours and phenylpropanolamine concentrations remained greater than 180 ng/mL for 12 hours. /Phenylpropanolamine hydrochloride/

Animal studies indicate that phenylpropanolamine is distributed into various tissues and fluids, including /cerebrospinal fluid/ and brain. /Phenylpropanolamine hydrochloride/

The bioavailability and pharmacokinetics of phenylpropanolamine hydrochloride from a controlled release caplet and solution were studied in 12 male subjects, aged 18 to 36 yr, who received either a 75 mg caplet once daily or a 25 mg solution 3 times daily for 4 days. Maximum plasma concentrations, time to maximum concentration, and areas under the concentration-time curves are reported for both caplet and solution. The mean first order absorption rate constant, elimination half-life and lag time for the drug from the caplet were 0.488 ngxhr/mL, 5.84 hr, and 0.394 hr, respectively, and 2.87 ngxhr/mL, 3.73 hr, and 0.325 hr, respectively, from the solution. The smaller apparent mean first order absorption rate constant and longer elimination half-life from the caplet is due to the slow release of drug, thereby slowing its absorption and producing sustained plasma drug concentrations.

For more Absorption, Distribution and Excretion (Complete) data for PHENYLPROPANOLAMINE (6 total), please visit the HSDB record page.

Used as a raw material in cold and diet tablets /Hydrochloride/

THERAP CAT: Decongestant (nasal); anorexic; in treatment of urinary incontinence

THERAP CAT (vet): In treatment of urinary incontinence in cats and dogs; decongestant (nasal)

MEDICATION

The Food and Drug Administration (FDA) is issuing a public health advisory concerning phenylpropanolamine hydrochloride. This drug is widely used as a nasal decongestant (in over-the-counter and prescription drug products) and for weight control (in over-the-counter drug products). FDA is taking steps to remove phenylpropanolamine from all drug products and has requested that all drug companies discontinue marketing products containing phenylpropanolamine. Phenylpropanolamine has been marketed for many years. A recent study reported that taking phenylpropanolamine increases the risk of hemorrhagic stroke (bleeding into the brain or into tissue surrounding the brain) in women. Men may also be at risk. Although the risk of hemorrhagic stroke is very low, FDA recommends that consumers not use any products that contain phenylpropanolamine.

Mucron

Rhindecon

Super Odrinex

Phenylpropanolamine hydrochloride preparations.；Table: Phenylpropanolamine Hydrochloride Preparations [Table#6022]

Phenylpropanolamine hydrochloride combination preparations.；Table: Phenylpropanolamine Hydrochloride Combinations [Table#6023]

Phenylpropanolamine, its salts, optical isomers, and salts of optical isomers

A chemical specified by regulation that, in addition to legitimate uses, is used in manufacturing a controlled substance in violation of the Act and is important to the manufacture of a controlled substance. (21 eCFR 1310.02)

Benzenemethanol, .alpha.-[(1S)-1-aminoethyl]-, (.alpha.R)-: ACTIVE

Benzenemethanol, .alpha.-[(1R)-1-aminoethyl]-, (.alpha.S)-rel-: INACTIVE

Phenylpropanolamine is used clinically as a decongestant and an anorectic. On the street it may be sold illegally in "speed" look-alikes. The "speed" look-alikes often contain up to 50 mg of phenylpropanolamine as well as ephedrine and caffeine. Some of the slang names for these drugs are "pink ladies," "black beauties," and "speckled pups."

Present in a number of common diet aids and nasal decongestants having such names as Dexatrim, Contac, and Dimetapp.