(±)-Trihexyphenidyl

301.47

301.47

205-614-4

12268

DTXSID4023705

N04AA01|N - Nervous system

2933399090

23.5

4.5

Solid

0.9941 (rough estimate)

114.3-115.0 °C

442.59°C (rough estimate)

211ºC

1.5614 (estimate)

3.14e-03 g/L

Trihexyphenidyl hydrochloride tablets should be stored in tight containers at 15-30 deg C. Trihexyphenidyl hydrochloride elixir should be stored at controlled room temperature (20-25 deg C); freezing of the elixir should be avoided.

5.61X10-10 mm Hg at 25 deg C (est)

LD50 ipr-mus: 150 mg/kg ARZNAD 21,1727,71

Henry's Law constant = 4.73X10-10 atm-cu m/mol at 25 °C (est)

pKa = 9.86 (est)

175.1 Ų [M+H]+ [CCS Type: DT, Method: single field calibrated]

Hydroxyl radical reaction rate constant = 1.29X10-14 cu cm/molec-sec at 25 °C (est)|White or slightly off white, crystalline powder ... very faint odor /Hydrochloride/|Crystals from isopropyl alcohol; mp: 264 °C; specific optical rotation: -30 deg at 20 °C/D (c = 0.4% in chloroform). Specific optical rotation: -25 deg at 20 °C/D (c = 0.4% in ethanol). /L-form hydrochloride/|Free base mp 112-113 °C. /L-form/

P264, P270, P301+P310, P321, P330, P405, P501

H301

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 trihexyphenidyl hydrochloride, approved on the basis of safety and effectiveness by FDA under sections 505 of the Federal Food, Drug, and Cosmetic Act. /Trihexyphenidyl hydrochloride/

Symptoms of overdose include mydriasis, dryness of mucous membranes, red face, atonic states of bowels and bladder, and hyperthermia in high doses. Trihexyphenidyl causes agitation, confusion, and hallucinations due to its effects on the central nervous system. Untreated overdose may result in death, especially in children. Respiratory depression and cardiac arrest may be seen as premortal signs.

Trihexyphenidyl has not been reported to cause serum aminotransferase elevations, but it has not been evaluated for effects on serum enzyme levels in a prospective manner. Trihexyphenidyl was cited as the cause of two cases of acute liver injury resulting in death in the Japanese literature, but few details were given and there have been no other reports of such injury in the literature in the subsequent 40 years. Thus, trihexyphenidyl must be a very rare cause of liver injury, if it occurs at all.

When trihexyphenidyl hydrochloride is used concomitantly with levodopa, the usual dose of each may need to be reduced. Careful adjustment is necessary, depending on side effects and degree of symptoms control. /Trihexylphenidyl hydrochloride/|...CENTRALLY ACTING ANTICHOLINERGIC AGENTS THAT MAY EXACERBATE TARDIVE DYSKINESIA /CAUSED BY CHLORPROMAZINE/ INCL...TRIHEXYPHENIDYL.|Trihexyphenidyl, applied in doses of 30 and 50 mg/kg (ip), did not influence the electroconvulsive threshold per se but when combined with valproate, strongly enhanced its anticonvulsant activity against maximal electroshock-induced seizures /in mice/ lowering the ED50 from 206 to 103 and 46 mg/kg, respectively. The chimney test and retention testing in mice revealed that administration of ... trihexyphenidyl at 30 mg/kg (ip) together with valproate in doses of 130 or 103 mg/kg (ip), respectively, resulted in motor impairment and caused impairment of long-term memory, similar to the effects of valproate alone, when applied at its ED50 against maximal electroshock. ... trihexyphenidyl /did not/ alter the total level of valproate in plasma. ...

The /apolipoprotein E/ epsilon4 allele in healthy elderly was associated with increased subjective mental slowing after trihexyphenidyl anticholinergic challenge.

Indicated for the treatment of parkinson's disease and extrapyramidal reactions caused by drugs.|FDA Label

Trihexyphenidyl is an oral anticholinergic agent used predominantly in the symptomatic therapy of Parkinson disease and movement disorders. Trihexyphenidyl has not been associated with serum enzyme elevations during treatment, but has been implicated in rare cases of acute liver injury.

Antiparkinson Agents

Anti-Dyskinesia Agents; Antiparkinson Agents; Muscarinic Antagonists; Parasympatholytics|Trihexyphenidyl hydrochloride is used for the adjunctive treatment of all forms of parkinsonian syndrome including the postencephalitic, arteriosclerotic, and idiopathic types. Trihexyphenidyl is also used for the relief of parkinsonian signs and symptoms of antipsychotic agent-induced (e.g., butyrophenones, phenothiazines, thioxanthenes) extrapyramidal effects. /Trihexylphenidyl hydrochloride/|Clinical results from preliminary trials with trihexyphenidyl in the treatment of other dyskinesias, Huntington's chorea, spasmodic torticollis, and associated disorders have been equivocal.|Trihexyphenidyl may also be effective in diminishing the frequency and duration of oculogyric crises, in decreasing salivation, in reducing spastic contractions and involuntary movements characteristic of dyskinesia, and in relieving mental inertia and depression characteristic of all forms of parkinsonian syndrome. As with other antiparkinsonian drugs, tolerance to trihexyphenidyl may develop during prolonged use. The maximum therapeutic response attainable with trihexyphenidyl is in the range of 20-30% symptomatic improvement in 50-75% of patients. Frequently, the maximum response requires empiric combination of trihexyphenidyl with other antimuscarinic drugs or with antihistaminic or dopaminergic agents. Some clinicians believe trihexyphenidyl to be of little value, but the majority have found it a useful adjunct in the multidimensional therapeutic approach to parkinsonian syndrome. Trihexyphenidyl is effective as adjunctive therapy for parkinsonian syndrome in patients receiving levodopa.|/EXPL THER/ The influence of two anticholinergic drugs (atropine, trihexyphenidyle) on the effectiveness of antidotal treatment to eliminate soman-induced lethal effects and convulsions was studied in rats. The oxime HI-6 when combined with centrally acting anticholinergic drug trihexyphenidyle seems to be more efficacious in the elimination of acute toxic effects of soman than its combination with atropine. The findings support the hypothesis that the choice of the anticholinergic drug is important for the effectiveness of antidotal mixture in the case of antidotal treatment of soman-induced acute poisoning.

Adverse reactions to trihexyphenidyl are mainly extensions of its anticholinergic effects. Adverse effects of trihexyphenidyl, which are experienced by 30-50% of patients receiving the drug, may include dryness of the mouth, dizziness, blurred vision, nausea, and nervousness. Other adverse effects typical of those produced by antimuscarinic drugs include constipation, tachycardia, mydriasis, urinary hesitancy or retention, drowsiness, increased intraocular tension, weakness, vomiting, and headache. CNS stimulation, usually manifested by restlessness, agitation, confusion, delirium, and hallucination or euphoria may occur with high dosage, or in persons with a history of hypersensitivity to other drugs, or in patients with arteriosclerosis. Isolated instances of rashes, dilatation of the colon, paralytic ileus, and suppurative parotitis secondary to dryness of the mouth have been reported. Angle-closure glaucoma has reportedly occurred in patients receiving prolonged therapy with trihexyphenidyl. Rarely, psychiatric disturbances such as delusion, amnesia, depersonalization, a sense of unreality, and one possible case of paranoia have been reported with trihexyphenidyl. The incidence and severity of adverse effects are generally dose related and adverse effects may occasionally be obviated by reduction in dosage. If a severe reaction occurs, the drug should be discontinued for several days and then readministered at a lower dosage.|Trihexyphenidyl should be used with caution or may be contraindicated in patients with conditions in which anticholinergic effects are undesirable. The usual precautions and contraindications associated with antimuscarinics should be observed with trihexyphenidyl.|Tardive dyskinesia may appear in some patients on long-term therapy with antipsychotic drugs or may occur after therapy with these drugs has been discontinued. Antiparkinsonism agents do not alleviate the symptoms of tardive dyskinesia and, in some instances, may aggravate them. However, parkinsonism and tardive dyskinesia often coexist in patients receiving chronic neuroleptic treatment, and anticholinergic therapy with trihexyphenidyl HCl may relieve some of these parkinsonism symptoms. /Trihexyphenidyl hydrochloride/|Since the use of trihexyphenidyl hydrochloride may, in some cases, continue indefinitely and since it has atropine-like properties, patients should be subjected to constant and careful long-term observation to avoid allergic and other untoward reactions. Inasmuch as trihexyphenidyl hydrochloride possesses some parasympatholytic activity, it should be used with caution in patients with glaucoma, obstructive disease of the gastrointestinal or genitourinary tracts, and in elderly males with possible prostatic hypertrophy. Geriatric patients, particularly over the age of 60, frequently develop increased sensitivity to the actions of drugs of this type, and hence, require strict dosage regulation. Incipient glaucoma may be precipitated by parasympatholytic drugs such as trihexyphenidyl hydrochloride. /Trihexyphenidyl hydrochloride/|For more Drug Warnings (Complete) data for TRIHEXYPHENIDYL (10 total), please visit the HSDB record page.

Trihexyphenidyl is an anticholinergic used in the symptomatic treatment of all etiologic groups of parkinsonism and drug induced extrapyramidal reactions (except tardive dyskinesia). Trihexyphenidyl possesses both anticholinergic and antihistaminic effects, although only the former has been established as therapeutically significant in the management of parkinsonism.

Agents used in the treatment of Parkinson's disease. The most commonly used drugs act on the dopaminergic system in the striatum and basal ganglia or are centrally acting muscarinic antagonists. (See all compounds classified as Antiparkinson Agents.)|Drugs that bind to but do not activate MUSCARINIC RECEPTORS, thereby blocking the actions of endogenous ACETYLCHOLINE or exogenous agonists. Muscarinic antagonists have widespread effects including actions on the iris and ciliary muscle of the eye, the heart and blood vessels, secretions of the respiratory tract, GI system, and salivary glands, GI motility, urinary bladder tone, and the central nervous system. (See all compounds classified as Muscarinic Antagonists.)

Trihexyphenidyl is rapidly absorbed from the gastrointestinal tract.|Using a sensitive radioreceptor assay for anticholinergic drugs, trihexyphenidyl /was assayed/ in human serum and ... its pharmacokinetics following short-term and long-term administration to patients with dystonia /was studied/. Previously untreated patients had a biphasic semilogarithmic plot of serum concentration-time consisting of an initial rapid distribution phase and a later slower elimination phase. Patients on long-term treatment showed only the slower elimination phase. Elimination followed first-order kinetics and was rapid, with a half-life of 3.7 + or - 0.4 (SEM) hours. There was no relationship between half-life and peak serum level, age, duration of therapy, or etiology or severity of dystonia. Although acute anticholinergic side effects paralleled the rise and fall of serum anticholinergic levels, the response of dystonia did not.|Trihexyphenidyl is rapidly absorbed from the GI tract. Following oral administration of trihexyphenidyl hydrochloride tablets, the onset of action occurs within 1 hour, peak effects last 2-3 hours, and the duration of action is 6-12 hours. The metabolic fate of trihexyphenidyl has not been determined; the drug is excreted in the urine, probably as unchanged drug. /Trihexylphenidyl hydrochloride/|The subcellular distribution of biperiden (BP), trihexyphenidyl (TP) and (-)-quinuclidinyl benzylate (QNB) in brain, heart and lung following high dose (3.2 mg/kg) iv administration was investigated in rats. The subcellular distribution of BP or TP used clinically conformed with that of QNB, a typical potent central muscarinic antagonist. The concentration-time courses of the brain subcellular fractions for these drugs were of two types which decreased slowly and in parallel to the plasma concentration. The subcellular distribution in the brain and heart was dependent on the protein amount of each fraction. The percent post-nuclear fraction (P2) of the total concentration in the lung was characteristically about 3-5 times larger than that in the heart. It was elucidated that the distribution in the lung differs from that in the brain and heart, with high affinity which is not dependent on the protein amount in the P2 fraction containing lysosomes. On the other hand, at a low dose (650 ng/kg) of 3H-QNB, each fraction as a percentage of the total concentration in the brain increased in synaptic membrane and synaptic vesicles and decreased in nuclei and cytosol as compared with the high dose. These results show that although the tissue concentration-time courses of anticholinergic drugs appear to decrease simply in parallel to plasma concentration, the subcellular distribution exhibits a variety of patterns among various tissues.|Twenty-four male subjects were randomized to receive two oral dosage forms of trihexyphenidyl HCl (alpha-cyclohexyl-alpha-phenyl-1-piperidinepropanol HCl). The dosage regimens were (1) a 5-mg immediate release (IR) tablet given twice daily at time zero and 12 hr later, and (2) two 5-mg sustained-release (SR) capsule formulations given daily. The number of adverse experiences following the SR formulation were approximately 50% of those for the IR formulation, the peak concentration (Cmax) after the SR formulation was significantly lower (p less than 0.05) than that after the first dose of the IR formulation, and the time to reach Cmax (tmax) was significantly longer after the SR formulation (p less than 0.05). The SR formulation maintained serum concentrations above 50, 60, and 70% of Cmax values for average time periods of 11.7, 9.4, and 5.9 hr, respectively, compared with values of 1.8, 1.2, and 0.9 hr after the IR formulation; the differences were all significant (p less than 0.05). The mean elimination half-life (t1/2) was similar (p greater than 0.05) after the SR (10.1 hr) and IR (8.7 hr) formulations. The statistical power of the study was 98.1% to detect a 20% difference in the area under the curve from time zero to time infinity (AUC0----infinity) between formulations. Although the AUC0----infinity after the SR formulation was statistically smaller (p less than 0.05) than after the IR tablet, the difference was less than 20%. Therefore, the SR formulation was bioequivalent to the IR tablet formulation of trihexyphenidyl. /Trihexylphenidyl hydrochloride/

Benzhexol and three of its metabolites excreted in urine in man have been investigated by glc.--mass spectrometry. Three isomeric hydroxylated metabolites were identified as the 1-(hydroxycyclohexyl)-1-phenyl-3-piperidinopropan-1-ols. 3. The amounts of benzhexol and its identified metabolites have been semiquantitatively determined after a single oral dose in two healthy adults. Approx. 56% of the dose was excreted as the hydroxylated metabolites. The levels of benzhexol excreted were too low to be measured by the techniques used.

3.3-4.1 hours|Twenty-four male subjects were randomized to receive two oral dosage forms of trihexyphenidyl HCl (alpha-cyclohexyl-alpha-phenyl-1-piperidinepropanol HCl). The dosage regimens were (1) a 5-mg immediate release (IR) tablet given twice daily at time zero and 12 hr later, and (2) two 5-mg sustained-release (SR) capsule formulations given daily. ... The mean elimination half-life (t1/2) was similar (p greater than 0.05) after the SR (10.1 hr) and IR (8.7 hr) formulations. /Trihexylphenidyl hydrochloride/|Using a sensitive radioreceptor assay for anticholinergic drugs, trihexyphenidyl /was assayed/ in human serum and ... its pharmacokinetics following short-term and long-term administration to patients with dystonia /was studied/. ... Elimination followed first-order kinetics and was rapid, with a half-life of 3.7 + or - 0.4 (SEM) hours. There was no relationship between half-life and peak serum level, age, duration of therapy, or etiology or severity of dystonia. ...

Trihexyphenidyl is a non-selective muscarinic acetylcholine receptor antagonist but binds with higher affinity to the M1 subtype. In vivo studies have shown that trihexyphenidyl demonstrates higher affinity for central muscarinic receptors located in the cerebral cortex and lower affinity for those located peripherally. Other studies suggest that trihexyphenidyl may modify nicotinic acetylcholine receptor neurotransmission, leading indirectly to enhanced dopamine release in the striatum. Although the anticholinergic has proven to be useful in the treatment of symptoms associated with Parkinson’s disease or other movement disorders, its mechanism of action has yet to be fully elucidated.|Cerebral blood flow and oxygen metabolism were studied in six previously untreated patients with Parkinson's disease (PD) before and after anticholinergic treatment using positron emission tomography (PET) and compared with six controls. The PET study and an assessment of the disability and cognitive impairment were performed before and after administration of 6 mg trihexyphenidyl for 5 to 11 weeks. All PD patients showed improvements in motor symptoms after the trihexyphenidyl treatment. Cognitive function did not significantly differ between before and after trihexyphenidyl treatment. However, after trihexyphenidyl treatment, regional cerebral blood flow (rCBF) and regional oxygen metabolic rate (rCMRO2) decreased by 15% in the striatum and by 10% in all cortical areas contralateral to predominantly symptomatic limbs, and by 10% in the ipsilateral striatum and all cortical areas, significantly below the values of controls in most cerebral cortices and striatum. These findings suggest that trihexyphenidyl inhibits the cortical cholinergic system and significantly decreases rCBF and rCMRO2 in the cerebral cortices without cognitive impairment in untreated patients with PD.|In common with other antimuscarinic agents, trihexyphenidyl produces an atropine-like blocking action on parasympathetic-innervated peripheral structures, including smooth muscle. In addition, trihexyphenidyl exhibits a direct spasmolytic action on smooth muscle and exhibits weak mydriatic, antisialagogue, and cardiovagal blocking effects. The exact mechanism of action of trihexyphenidyl in parkinsonian syndrome is not understood but may result from blockade of efferent impulses and from central inhibition of cerebral motor centers. In small doses, trihexyphenidyl depresses the CNS but larger doses cause cerebral excitement resembling the signs of atropine toxicity.|In vivo microdialysis was used to study the effect of the non-selective muscarinic antagonist, trihexyphenidyl, on the decarboxylation of levodopa (L-dopa) in the striatum of hemi-Parkinson rats. In normal rats, continuous perfusion of trihexyphenidyl (1 mM) via the microdialysis probe induced a significant increase in striatal dopamine release, followed by a decrease to below baseline values. A similar effect was observed, though less pronounced, in denervated striatum of rats with a unilateral 6-hydroxydopamine lesion of the nigrostriatal pathway. In these hemi-Parkinson rats, continuous striatal perfusion of trihexyphenidyl had no effect on the biotransformation of locally applied L-dopa (2 uM for 20 min) to dopamine in either intact or denervated striatum. However, systemic administration of trihexyphenidyl (1.5 mg/kg ip) produced an attenuation of the L- dopa-induced dopamine release in the intact striatum (contralateral to the lesion) of hemi-Parkinson rats. This effect was absent in the denervated striatum of these animals. We confirmed that L-dopa induces an increase in striatal dopamine output which is influenced by the severity of the dopaminergic denervation. The absence of an effect of trihexyphenidyl locally applied in the striatum, on biotransformation of L-dopa suggests that the site of action of antimuscarinic drugs may not be in the striatum and, therefore, remains unclear.

1-phenyl-3-(piperidine-1-yl)propan-1-one

Emergency and supportive measures: Maintain an open airway and assist ventilation if needed. Treat hyperthermia, coma, rhabdomyolysis, and seizures if they occur. /Anticholinergics/|Specific drugs and antidotes: A small dose of physostigmine .... can be given to patients with severe toxicity (e.g., hyperthermia, severe delirium, or tachycardia). Caution: Physostigmine can cause AV block, asystole, and seizures, especially in patients with tricyclic antidepressant overdose. Neostigmine, a peripherally acting cholinesterase inhibitor, may be useful in treating anticholinergic-induced ileus. /Anticholinergics/|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. Because of slowed gastrointestinal motility, gut decontamination procedures may be helpful even in late-presenting patients. /Anticholinergics/|Enhanced elimination: Hemodialysis, hemoperfusion, peritoneal dialysis, and repeat-dose charcoal are not effective in removing anticholinergic agents. /Anticholinergics/|For more Antidote and Emergency Treatment (Complete) data for TRIHEXYPHENIDYL (7 total), please visit the HSDB record page.

/SIGNS AND SYMPTOMS/ ... In a group of 22 psychiatric patients receiving long-term antipsychotic medication concurrently with trihexyphenidyl the effects of trihexyphenidyl withdrawal were studied double-blind and placebo controlled. Anxiety, psychotic symptoms, extrapyramidal symptoms and salivary flow were monitored. Blood pressure, pulse, sleep duration, weight and body temperature were recorded daily. The result was a recognizable withdrawal syndrome indicated by an increase in anxiety with various physical complaints, as well as evidence of orthostatic hypotension and tachycardia. A temporary deterioration was noted in psychotic symptomatology and extrapyramidal symptoms. The majority of the parameters regained baseline values, indicating the symptoms were related to the discontinuation of trihexyphenidyl and supporting the existence of a withdrawal syndrome.|/SIGNS AND SYMPTOMS/ In Brazil, the medicinal misuse of trihexyphenidyl has been observed among several segments of society. The present study was conducted in the city of Sao Paulo during 2002 to characterize this abuse. A sample of 21 users and 16 ex-users was interviewed using qualitative methodology; the subjects were single, unemployed, male polydrug users, who used trihexyphenidyl in order to attain states of mental alterations, mainly hallucinations and deliriums. Trihexyphenidyl is consumed in association with alcohol, other licit drugs (benzodiazepines), or illicit drugs, impairing cognitive functions such as memory, attention, and learning, intervening with some activities of users' daily life.|/CASE REPORTS/ ... Two case reports of trihexyphenidyl abuse /are described/. In one of the cases a double-blind, placebo-controlled withdrawal was conducted and monitored on a number of physiological parameters and the Hamilton Anxiety Rating Scale. A recognizable withdrawal syndrome followed discontinuation of the drug. ...|/CASE REPORTS/ ... The case presented is of anti-cholinergic abuse by a chronic schizophrenic who abused trihexyphenidyl, up to 200 mg per day, to achieve an euphoric effect. The drug was partly prescribed in psychiatric clinics, but mostly bought in the drugstore. The discontinuance of trihexyphenidyl produced anxiety, which was relieved by anxiolytics. The patient also feigned extrapyramidal symptoms to get anticholinergic injections during drug abstinence. ...|For more Human Toxicity Excerpts (Complete) data for TRIHEXYPHENIDYL (13 total), please visit the HSDB record page.

Apo Trihex

Trade Names. Artane (Lederle), Bentex (Steinhard), Broflex (Bio-Med), Pargitan (KabiVitrum), Parkinane (Lederle), Triphenidone (Toho). /Trihexylphenidyl hydrochloride/|Oral: Elixir: 2 mg/5 mL Trihexyphenidyl Hydrochloride Elixir (Mikart), (Pharmaceutical Associates), (Pharmaceutical Ventures). Tablets: 2 mg Trihexyphenidyl Hydrochloride Tablets (URL), (Vintage), (Watson), (West-Ward); 5 mg Trihexyphenidyl Hydrochloride Tablets (URL), (Vintage), (Watson), (West-Ward). /Trihexypheridyl hydrochloride/

TRIHEXYPHENIDYL MAY BE COMBINED WITH OTHER ANTIPARKINSONIAN DRUGS.

CHROMATOGRAPHIC DATA FOR METHADONE & RELATED DRUGS; GLC RETENTION TIMES RELATIVE TO TRIHEXYLPHENIDYL & RF VALUES IN TLC SYSTEM FOR COMMON BASIC DRUGS LIKELY TO BE PRESENT IN POISONING INCIDENTS. /FROM TABLE/|FLUORIMETRIC PROCEDURE IS DESCRIBED FOR DETECTION OF ARTANE (TRIHEXYLPHENIDYL HYDROCHLORIDE) IN TABLET FORMULATIONS. /Trihexylphenidyl hydrochloride/|Analyte: trihexyphenidyl hydrochloride; matrix: chemical identification; procedure: infrared absorption spectrophotometry with comparison to standards /trihexyphenidyl hydrochloride/|Analyte: trihexyphenidyl hydrochloride; matrix: chemical identification; procedure: retention time of the major peak of the liquid chromatogram with comparison to standards /trihexyphenidyl hydrochloride/|For more Analytic Laboratory Methods (Complete) data for TRIHEXYPHENIDYL (12 total), please visit the HSDB record page.

Analyte: trihexyphenidyl; matrix: blood (plasma, whole); procedure: high-performance liquid chromatography with ultraviolet detection at 254 nm; limit of detection: 10 ng/mL|Analyte: trihexyphenidyl; matrix: blood (plasma); procedure: high-performance liquid chromatography with electrochemical detection|Analyte: trihexyphenidyl; matrix: blood (serum, whole), tissue (liver); procedure: high-performance liquid chromatography with ultraviolet detection at 220 nm|Analyte: trihexyphenidyl; matrix: blood (whole), urine; procedure: high-performance liquid chromatography with ultraviolet detection at 200.5 nm

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