Ractopamine

301.38

301.38

57370OZ3P1

DTXSID7048378

2922502000

72.72000

3.13300

off-white or light-yellow powder

1.189

165-167°C

520.5±50.0 °C(Predicted)

165.3ºC

1.608

In water, 4.1X10+3 mg/L at 25 °C (est)

6.4X10-11 at 25 °C (est)

9.97±0.26

Henry's Law constant = 1.3X10-19 atm-cu m/mol at 25 °C (est)

pKa = 9.4 (secondary amine) (est)

168.9 Ų [M+H]+ [CCS Type: TW]|168.35 Ų [M-H]-

Mol wt 301.38. Mixture of 4 stereoisomers in approx equal proportions. Product containing 51% RR,SS- and 49% RS,SR-diastereomers, mp 124-129 °C /Hydrochloride/|Hydroxyl radical reaction rate constant = 1.9X10-10 cu cm/molecule-sec at 25 °C (est)

20/22-43

24-26-37

Xn

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.

New animal drugs for use in animal feeds. Ractopamine. Conditions of use: (1) Swine: ... For increased rate of weight gain, improved feed efficiency, and increased carcass leanness in finishing swine fed a complete ration containing at least 16 percent crude protein from 150 lb (68 kg) to 240 lb (109 kg) body weight. Limitations: Feed continuously as sole ration. ... For improved feed efficiency and increased carcass leanness in finishing swine fed a complete ration containing at least 16 percent crude protein from 150 lb (68 kg) to 240 lb (109 kg) body weight. Limitations: Feed continuously as sole ration ... (2) Cattle: ... cattle fed in confinement for slaughter: For increased rate of weight gain and improved feed efficiency during the last 28 to 42 days on feed. Limitations: Feed continuously as sole ration during the last 28 to 42 days on feed. Not for animals intended for breeding. ... Cattle fed in confinement for slaughter: For increased rate of weight gain, improved feed efficiency, and increased carcass leanness during the last 28 to 42 days on feed. Limitations: Feed continuously as sole ration during the last 28 to 42 days on feed. Not for animals intended for breeding. /May be used in combination with tylosin and monesin/|New animal drugs for use in animal feeds. Requirement of a medicated feed mill license. Ractopamine is included on this list.|The Generic Animal Drug and Patent Restoration act requires that each sponsor of an approved animal drug must submit to the FDA certain information regarding patents held for the animal drug or its method of use. The Act requires that this information, as well as a list of all animal drug products approved for safety and effectiveness, be made available to the public. Ractopamine hydrochloride is included on this list. /Ractopamine hydrochloride/

An 8-wk study of the effects of CLA, rendered animal fats, and ractopamine, and their interactive effects on growth, fatty acid composition, and carcass quality of genetically lean pigs was conducted. Gilts (n = 228; initial BW of 59.1 kg) were assigned to a 2 x 2 x 3 factorial arrangement consisting of CLA, ractopamine, and fat treatments. The CLA treatment consisted of 1% CLA oil (CLA-60) or 1% soybean oil. Ractopamine levels were either 0 or 10 ppm. Fat treatments consisted of 0% added fat, 5% choice white grease (CWG), or 5% beef tallow (BT). The CLA and fat treatments were initiated at 59.1 kg of BW, 4 wk before the ractopamine treatments. The ractopamine treatments were imposed when the gilts reached a BW of 85.7 kg and lasted for the duration of the final 4 wk until carcass data were collected. Lipids from the belly, outer and inner layers of backfat, and LM were extracted and analyzed for fatty acid composition from 6 pigs per treatment at wk 4 and 8. Feeding CLA increased (P < 0.02) G:F during the final 4 wk. Pigs fed added fat as either CWG or BT exhibited decreased (P < 0.05) ADFI and increased (P < 0.01) G:F. Adding ractopamine to the diet increased (P < 0.01) ADG, G:F, and final BW. The predicted carcass lean percentage was increased (P < 0.05) in pigs fed CLA or ractopamine. Feeding either 5% fat or ractopamine increased (P < 0.05) carcass weight. Adding fat to the diets increased (P < 0.05) the 10th rib backfat depth but did not affect predicted percent lean. Bellies of gilts fed CLA were subjectively and objectively firmer (P < 0.01). Dietary CLA increased (P < 0.01) the concentration of saturated fatty acids and decreased (P < 0.01) the concentration of unsaturated fatty acids of the belly fat, both layers of backfat, and LM. Ractopamine decreased (P < 0.01) the i.m. fat content of the LM but had relatively little effect on the fatty acid profiles of the tissues compared with CLA. These results indicate that CLA, added fat, and ractopamine work mainly in an additive fashion to enhance pig growth and carcass quality. Furthermore, these results indicate that CLA results in more saturated fat throughout the carcass.

The objectives of this study were to measure the residues of ractopamine in livers and kidneys of cattle (n = 6), sheep (n = 6), and ducks (n = 9) after treatment with dietary ractopamine for seven (sheep, ducks) or eight (cattle) consecutive days and to measure the depletion of ractopamine from urine of cattle and sheep. ... Analysis was performed with HPLC using fluorescence detection after liquid- (hydrolyzed samples) and(or) solid-phase extraction. No residues were detected in duck tissues. Liver residues in sheep averaged 24.0 and 2.6 ppb after 0- and 3-day withdrawal periods, respectively. Sheep liver residues after a 7-day withdrawal period were less than the limit of quantification (2.5 ppb). Sheep kidney residues were 65.1 and undetectable at 0- and at 3- and 7-day, withdrawal periods, respectively. Cattle liver residues were 9.3, 2.5, and undetectable after 0-, 3-, and 7-day withdrawal periods, respectively; kidney residues were 97.5, 3.4, and undetectable at the same respective withdrawal periods.

Mesh Heading: Adrenergic beta-agonists|MEDICATION (VET): Animal growth promotant|MEDICATION (VET): The effects of the beta-agonist ractopamine, approved for use in finishing swine and cattle to improve carcass quality and performance, were examined on two important foodborne pathogens, Escherichia coli O157:H7 and Salmonella. Ractopamine, administered to sheep before and after oral inoculation with E. coli O157:H7, increased (P < 0.01) fecal shedding and tended to increase (P = 0.08) cecal populations of the challenge strain. Pigs receiving ractopamine in the diet and then experimentally infected with Salmonella Typhimurium, had decreased (P < 0.05) fecal shedding and fewer (P = 0.05) liver samples positive for the challenge strain of Salmonella. Pure cultures of E. coli O157:H7 (used in the present sheep study), E. coli O157:H19 (isolated from pigs with postweaning diarrhea), Salmonella Typhimurium (used in the present pig study), and Salmonella Choleraesuis were incubated with varying concentrations of ractopamine to determine if ractopamine has a direct effect on bacterial growth. No differences in growth rate were observed for either strain of E. coli or for Salmonella Typhimurium when incubated with increasing concentrations of ractopamine. The growth rate for Salmonella Choleraesuis was increased with the addition of 2.0 ug ractopamine/ml compared with the other concentrations examined. Collectively, these results indicate that ractopamine may influence gut populations and fecal shedding of E. coli O157:H7 and Salmonella. Because ractopamine is currently approved to be fed to finishing cattle and swine immediately before slaughter, any potential for decreasing foodborne pathogens has exciting food safety implications.|MEDICATION (VET): An 8-wk study of the effects of CLA, rendered animal fats, and ractopamine, and their interactive effects on growth, fatty acid composition, and carcass quality of genetically lean pigs was conducted. Gilts (n = 228; initial BW of 59.1 kg) were assigned to a 2 x 2 x 3 factorial arrangement consisting of CLA, ractopamine, and fat treatments. The CLA treatment consisted of 1% CLA oil (CLA-60) or 1% soybean oil. Ractopamine levels were either 0 or 10 ppm. Fat treatments consisted of 0% added fat, 5% choice white grease (CWG), or 5% beef tallow (BT). The CLA and fat treatments were initiated at 59.1 kg of BW, 4 wk before the ractopamine treatments. The ractopamine treatments were imposed when the gilts reached a BW of 85.7 kg and lasted for the duration of the final 4 wk until carcass data were collected. Lipids from the belly, outer and inner layers of backfat, and LM were extracted and analyzed for fatty acid composition from 6 pigs per treatment at wk 4 and 8. Feeding CLA increased (P < 0.02) G:F during the final 4 wk. Pigs fed added fat as either CWG or BT exhibited decreased (P < 0.05) ADFI and increased (P < 0.01) G:F. Adding ractopamine to the diet increased (P < 0.01) ADG, G:F, and final BW. The predicted carcass lean percentage was increased (P < 0.05) in pigs fed CLA or ractopamine. Feeding either 5% fat or ractopamine increased (P < 0.05) carcass weight. Adding fat to the diets increased (P < 0.05) the 10th rib backfat depth but did not affect predicted percent lean. Bellies of gilts fed CLA were subjectively and objectively firmer (P < 0.01). Dietary CLA increased (P < 0.01) the concentration of saturated fatty acids and decreased (P < 0.01) the concentration of unsaturated fatty acids of the belly fat, both layers of backfat, and LM. Ractopamine decreased (P < 0.01) the i.m. fat content of the LM but had relatively little effect on the fatty acid profiles of the tissues compared with CLA. These results indicate that CLA, added fat, and ractopamine work mainly in an additive fashion to enhance pig growth and carcass quality. Furthermore, these results indicate that CLA results in more saturated fat throughout the carcass.|For more Therapeutic Uses (Complete) data for RACTOPAMINE (8 total), please visit the HSDB record page.

Drugs that selectively bind to and activate beta-adrenergic receptors. (See all compounds classified as Adrenergic beta-Agonists.)

/The authors/ investigated the detection, confirmation, and metabolism of the beta-adrenergic agonist ractopamine administered as Paylean to the horse. ... Based on the quantitation ions for ractopamine standards extracted from urine, standard curves showed a linear response for ractopamine concentrations between 10 and 100 ng/mL with a correlation coefficient r > 0.99, whereas standards in the concentration range of 10-1000 ng/mL were fit to a second-order regression curve with r > 0.99. ... Urine concentration of parent ractopamine 24 h post-dose was measured at 360 ng/mL by GC-MS after oral administration of 300 mg. Urinary metabolites were identified by electrospray ionization (+) tandem quadrupole mass spectrometry and were shown to include glucuronide, methyl, and mixed methyl-glucuronide conjugates|In a bioavailability study that complied with good laboratory practice (GLP), groups of five male and five female rats were given [14C]ractopamine as a single oral dose at 0.5, 2.0, or 20 mg/kg bw by gavage. The amount of radiolabel was quantified in samples of plasma and whole blood collected for 24 hr after dosing. Comparison of the area under the curve (AUC) of concentration-time for plasma and whole blood indicated that the bioavailability of (14)C-ractopamine was proportional to dose for males and females at doses up to 2.0 mg/kg bw. Increasing the dose to 20 mg/kg bw resulted in an increase in AUC versus dose in males and, to a more pronounced degree, in females. The absolute bioavailability of (14)C-ractopamine in rats cannot be determined from the results of this study since (14)C-ractopamine was not administered intravenously for comparison of oral and intravenous AUC values.|Experiments were conducted to determine the total residues remaining in ocular tissues of cattle and turkeys after oral administration of (14)C-ractopamine HCl. Twelve cattle were intraruminally dosed with 0.9 mg /kg/d of (14C-)ractopamine HCl for 7 d. Four cattle each were slaughtered with withdrawal periods of 48, 96, and 144 hr. Radioactive residues were not detectable in whole-eye homogenates from the cattle. Eight male and eight female turkeys per treatment received either 7.5, 22.5, or 30 ppm dietary (14)C-ractopamine HCl (0.33, 1.02, and 1.36 mg/kg/d; treatment groups 1, 2, and 3, respectively) for 7 d, and the birds were slaughtered with a 0-d withdrawal period. Eyes were dissected into retina/choroid/schlera (RCS), cornea/iris (CI), and aqueous humor (AH) fractions. Residues in RCS, CI, and AH of treatment 1 turkeys were not detectable. Residues in AH were < 0.02 ppm in treatment groups 2 and 3. Mean residues in RCS ranged from 0.15 to 0.26 ppm, and mean CI residues ranged from <0.09 to 0.17 ppm for treatment groups 2 and 3, respectively.|Ractopamine HCl is a beta-adrenergic leanness-enhancing agent recently approved for use in swine. Depletion of ractopamine in tissues, and elimination of ractopamine and its metabolites in urine, is of interest for the detection of off-label use. The objectives of this study were to measure the residues of ractopamine in livers and kidneys of cattle (n = 6), sheep (n = 6), and ducks (n = 9) after treatment with dietary ractopamine for seven (sheep, ducks) or eight (cattle) consecutive days and to measure the depletion of ractopamine from urine of cattle and sheep. Two cattle and sheep and three ducks were each slaughtered with withdrawal periods of 0, 3, and 7 day. Urine samples were collected daily from cattle and sheep. Tissue ractopamine concentrations were determined using the regulatory method (FDA approved) for ractopamine in swine tissues. Ractopamine residues in urine samples were measured before and after hydrolysis of conjugates. Analysis was performed with HPLC using fluorescence detection after liquid- (hydrolyzed samples) and(or) solid-phase extraction. No residues were detected in duck tissues. Liver residues in sheep averaged 24.0 and 2.6 ppb after 0- and 3-day withdrawal periods, respectively. Sheep liver residues after a 7-day withdrawal period were less than the limit of quantification (2.5 ppb). Sheep kidney residues were 65.1 and undetectable at 0- and at 3- and 7-day, withdrawal periods, respectively. Cattle liver residues were 9.3, 2.5, and undetectable after 0-, 3-, and 7-day withdrawal periods, respectively; kidney residues were 97.5, 3.4, and undetectable at the same respective withdrawal periods. Concentrations of parent ractopamine in sheep urine were 9.8+ or - 3.3 ppb on withdrawal d 0 and were below the LOQ (5 ppb) beyond the 2-day withdrawal period. After the hydrolysis of conjugates, ractopamine concentrations were 5,272 + or - 1,361 ppb on withdrawal d 0 and 178 + or - 78 ppb on withdrawal d 7. Ractopamine concentrations in cattle urine ranged from 164+ or - 61.7 ng/mL (withdrawal d 0) to below the LOQ (50 ppb) on withdrawal day 4. After the hydrolysis of conjugates in cattle urine, ractopamine concentrations were 4,129+ or - 2,351 ppb (withdrawal day 0) to below the LOQ (withdrawal d 6). These data indicate that after the hydrolysis of conjugates, ractopamine should be detectable in urine of sheep as long as 7 day after the last exposure to ractopamine and as long as 5 day after withdrawal in cattle.|For more Absorption, Distribution and Excretion (Complete) data for RACTOPAMINE (16 total), please visit the HSDB record page.

In urine, only a minor fraction of radioactivity recovered was parent ractopamine. Swine excreted about 4-16% of the parent compound in the urine after a single oral dose of ractopamine. After repeated doses, the amount of unchanged drug increased to 36-85% of total radioactivity in the urine collected on day 4 of a 4-day dosing regimen. In rats injected with (14)C-ractopamine at 9 mg/kg bw intraperitoneally, parent drug represented 22.6% of total urinary radioactivity while only 1.9% of radioactivity was associated with unchanged ractopamine after an oral dose of 9.9 mg/kg bw. The greater proportion of parent drug in the urine after parenteral administration than after oral administration suggests that liver and intestine play an important role in the biotransformation of ractopamine after oral administration. Therefore, although well absorbed from the gastrointestinal tract, the systemic availability of parent ractopamine is reduced, owing to a significant first-pass metabolism.|In the bile of rats dosed orally with (14)C-ractopamine, at least seven different crude metabolite fractions were partitioned chromatographically. Four of the crude metabolite fractions representing 76% of biliary radioactivity were isolated and identified with a sulfate-ester/glucuronic acid diconjugate of ractopamine as the main metabolite (46% of total biliary radioactivity). A further 6% of radioactivity was identified as a monosulfate conjugate and 25% as monoglucuronides of ractopamine. The site of sulfation was established at the C-10' phenol (aromatic ring attached to carbinol). The sulfate conjugation was not stereospecific. The major site of glucuronidation was the C-10 phenol (phenol attached to the nitrogen substituent).|After a withdrawal of 6 hr (rats, dogs) or 12hr (swine, cattle), unchanged ractopamine represented 40, 14, 52, and 13-16% of the total extractable and identifiable residues in the rat, dog, pig, and cattle livers, respectively, and 21, 29, 28-30, and 14% in the kidneys, respectively. After a withdrawal of 24 hr and 72 hr, parent ractopamine represented 14.1% and 3.6% in liver, and 27.5% and 3% of total residues in kidney, respectively, in swine. The remaining residue was found to comprise conjugates of ractopamine. The chromatographic profiles of the (14)C-labelled residue extracts of rat, dog, pig, and cattle liver were qualitatively similar. The laboratory animals had generally a higher percentage of metabolites as residues. Studies in rats and dogs showed that urine from animals dosed with (14)C-ractopamine contained the same four glucuronide metabolites of ractopamine as in pigs. It is concluded that the dogs and rats used in the toxicological studies were exposed to the same metabolites as those found in the edible tissues of pigs and cattle.|In studies in rats, dogs, pigs, and cattle fed (14)C-ractopamine, a fourth metabolite was identified as a glucuronic acid diconjugate. The conjugation of the hydroxyl groups in both the aromatic ring attached to the carbinol and the phenol attached to the nitrogen substituent was not stereospecific.|For more Metabolism/Metabolites (Complete) data for RACTOPAMINE (8 total), please visit the HSDB record page.

The elimination half-life was about 6-7 hr.|The results of a study in six healthy male human volunteers receiving a single oral dose of 40 mg of ractopamine hydrochloride indicate a similar profile of pharmacokinetics and biotransformation in humans and animals. ... The half-life in plasma was about 4 hr.

The RR-isomer (butopamine) is the stereoisomer with the most activity at the b-adrenoceptor. Butopamine was shown to be a non-selective ligand at the beta1- and beta2-adrenoceptors, but signal transduction is more efficiently coupled through the b2-adrenoceptor than the b1- adrenoceptor. Therefore, the RR-isomer of ractopamine is considered to be a full agonist at the beta2-adrenoceptor and a partial agonist at the beta-adrenoceptor. These results are consistent with the pharmacological characterization of racemic ractopamine in isolated cardiac (atria) and smooth muscle (costo-uterine, vas deferens, trachea), which shows a maximal response at beta2- and a submaximal response at b1-adrenoceptors when compared with the full beta1- and beta2- adrenoceptor agonist isoproterenol.

/SRP:/ Basic treatment: Establish a patent airway (oropharyngeal or nasopharyngeal airway, if needed). Suction if necessary. Watch for signs of respiratory insufficiency and assist ventilations if needed. Administer oxygen by nonrebreather mask at 10 to 15 L/min. Monitor for pulmonary edema and treat if necessary ... . Monitor for shock and treat if necessary ... . Anticipate seizures and treat if necessary ... . For eye contamination, flush eyes immediately with water. Irrigate each eye continuously with 0.9% saline (NS) during transport ... . Do not use emetics. For ingestion, rinse mouth and administer 5 ml/kg up to 200 ml of water for dilution if the patient can swallow, has a strong gag reflex, and does not drool ... . Cover skin burns with dry sterile dressings after decontamination ... . /Poisons A and B/|/SRP:/ Advanced treatment: Consider orotracheal or nasotracheal intubation for airway control in the patient who is unconscious, has severe pulmonary edema, or is in severe respiratory distress. Positive-pressure ventilation techniques with a bag valve mask device may be beneficial. Consider drug therapy for pulmonary edema ... . Consider administering a beta agonist such as albuterol for severe bronchospasm ... . Monitor cardiac rhythm and treat arrhythmias as necessary ... . Start IV administration of D5W /SRP: "To keep open", minimal flow rate/. Use 0.9% saline (NS) or lactated Ringer's if signs of hypovolemia are present. For hypotension with signs of hypovolemia, administer fluid cautiously. Watch for signs of fluid overload ... . Treat seizures with diazepam or lorazepam ... . Use proparacaine hydrochloride to assist eye irrigation ... . /Poisons A and B/

/HUMAN EXPOSURE STUDIES/ The dose-dependent effects of ractopamine on the human cardiovascular system were studied in a limited number of human volunteers (six persons) given ascending single oral doses equal to 67, 133, 200, 333, and 597 ug/kg bw, with an interval of 48 h between doses. Occasional mild to moderate sensations of increase in heart rate and heart pounding were reported at doses of 200, 333, and 597 ug/kg bw. Dose dependent increases in heart rate and cardiac output, and shortened electromechanical systole, as measured by echocardiography, were observed. The changes appeared within the first hour after the administration of ractopamine and values gradually returned to those before treatment. The systolic blood pressure increased in a dose dependent manner. Unlike in monkeys and dogs, ractopamine had little effect on diastolic blood pressure in humans. Only minor cardiovascular effects were observed at 133 ug/kg bw. The NOELs for the relevant cardiac variables were 67 ug/kg bw for electromechanical systole, ventricular ejection time, and maximum velocity of circumferential fibre shortening, 133 ug/kg bw for heart rate and 200 ug/kg bw for cardiac output.|/SIGNS AND SYMPTOMS/ Adverse effects of prolonged therapeutic use of beta-agonists including tachycardia, vasodilation, skeletal muscle tremor, nervousness, metabolic disturbances, and beta-adrenoceptor desensitization are pharmacologically predictable, dose-related and potency-related. Non-pharmacological effects include airway hyper-responsiveness and increased airway inflammation. The incidence and severity of adverse reactions may vary for any given compound. The impact of the R- and S-enantiomers of beta-agonists on adverse effects remains unclear. /beta-Agonists/|/EPIDEMIOLOGY STUDIES/ The dose-response effect of ractopamine on the human cardiovascular system was studied in a single-blind, placebo-controlled, ascending single-dose protocol. The study was conducted with six healthy male volunteers (body weight: range, 67.8-79.6 kg; mean, 75.5 kg), given oral placebo plus five oral doses of 5, 10, 15, 25, and 40 mg of ractopamine, with a washout period of 48 h between doses. On a body-weight basis, the doses ranged from 0.063 to 0.590 mg/kg bw. Using standard and echocardiographic methods, measurements for 14 cardiovascular variables were obtained at nine hourly time-points in each subject. No serious adverse events were reported. At doses of 15, 25, and 50 mg, sensations of increase in heart rate were reported for two, three, and four men, and sensation of heart pounding in one, three, and one man, respectively. The adverse effects were considered to be treatment-related and to be either mild or moderate in severity. One man was withdrawn from the study after the 25 mg dose because of adverse cardiac effects. Dose-dependent changes of cardiac variables appeared within the first hour after administration of ractopamine and gradually returned to baseline values before treatment. At a dose of 5 mg, there was apparently no cardiovascular response, and at 10 mg only minor effects were reported. At 15, 25, and 40 mg, the heart rate was elevated about 20, 30, and 50 beats per min above control and the cardiac output increased by approximately 35%, 55%, and 90%, respectively. At the same doses, the electromechanical systole was shortened by about 10%, 14%, and 19%, respectively. The systolic blood pressure increased in a dose-dependent manner. In contrast to the vasodilative effects recorded in monkeys and dogs, ractopamine did not change or even increase the diastolic pressure.|/OTHER TOXICITY INFORMATION/ The Committee concluded that the response in monkeys is more predictive of the acute cardiovascular response in humans exposed to dietary ractopamine than is that in dogs. Monitoring in the studies in animals and humans was appropriately timed to reveal the onset, time-to-peak, and duration of ractopamine-induced cardiac effects. The time course of the cardiostimulatory effects of ractopamine was comparable in humans, monkeys, and dogs.|/OTHER TOXICITY INFORMATION/ The Committee reviewed publicly available literature on nontherapeutic effects in humans after long-term use of beta-adrenoceptor agonists. The reported side-effects of prolonged therapeutic use of beta-adrenoceptor agonists include tachycardia, vasodilation, skeletal muscle tremor, nervousness, metabolic disturbances (hyperglycaemia and hypokalaemia), and beta-adrenoceptor desensitization. These effects are pharmacologically predictable, dose-related and potencyrelated, with cardiovascular effects being the most commonly reported side-effects. Non-pharmacological effects include airway hyper-responsiveness and increased airway inflammation. The incidence and severity of side-effects varies for any given compound. Tolerance to pharmacologically-predictable, non-therapeutic effects occurs readily. There is no evidence for any increased incidence of smooth muscle tumors such as leiomyomas, or of any other tumors, among human users of these drugs. Little or no relaxant response to beta2-adrenoceptor agonists has been reported for the non-pregnant human uterus.

4-hydroxy-alpha-(((3-(4-hydroxyphenyl)-1-methylpropyl)amino)methyl)benzenemethanol

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