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debrisoquin

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Description

Debrisoquin is an antihypertensive drug that acts as a postsynaptic alpha-adrenergic receptor antagonist. It is synthesized through a series of steps involving the condensation of 2-chloro-4-methylaniline with 2-amino-5-nitrothiazole, followed by reduction and cyclization. Debrisoquin's mechanism of action involves blocking the release of norepinephrine at sympathetic nerve endings, leading to vasodilation and a decrease in blood pressure. It is also a potent inhibitor of cytochrome P450 2D6 (CYP2D6), an enzyme responsible for metabolizing a wide range of drugs. Debrisoquin's importance stems from its role in understanding the genetic basis of drug metabolism. Due to its unique metabolic profile, Debrisoquin has been extensively used as a probe drug to study CYP2D6 activity and polymorphism. Variations in CYP2D6 activity can lead to significant differences in drug response, highlighting the importance of pharmacogenetic testing. Debrisoquin itself is no longer widely used clinically due to its side effects, such as postural hypotension and dry mouth. However, its legacy continues to be felt in the field of pharmacogenetics, where it serves as a cornerstone for understanding individual drug metabolism and response.'

Debrisoquin: An adrenergic neuron-blocking drug similar in effects to GUANETHIDINE. It is also noteworthy in being a substrate for a polymorphic cytochrome P-450 enzyme. Persons with certain isoforms of this enzyme are unable to properly metabolize this and many other clinically important drugs. They are commonly referred to as having a debrisoquin 4-hydroxylase polymorphism. [Medical Subject Headings (MeSH), National Library of Medicine, extracted Dec-2023]

Cross-References

ID SourceID
PubMed CID2966
CHEMBL ID169901
CHEBI ID34665
SCHEMBL ID309184
MeSH IDM0005709

Synonyms (66)

Synonym
3,4-dihydro-2(1h)-isoquinoline carboxamidine sulfate
nsc139330
3,4-dihydroisoquinoline-2(1h)-carboximidamide
PRESTWICK2_000372
LOPAC0_000326
PRESTWICK3_000372
BSPBIO_000523
BPBIO1_000577
CHEBI:34665 ,
debrisoquina
debrisoquinum
sulfuric acid compound with 3,4-dihydro-2(1h)-isoquinolinecarboximidamide (1:1)
3,4-dihydro-1h-isoquinoline-2-carboxamidine
2(1h)-isoquinolinecarboxamidine, 3,4-dihydro-, sulfate (2:1)
1,2,3, 4-tetrahydro-isoquinoline-2-carboxamidine sulfate
1131-64-2
2(1h)-isoquinolinecarboxamidine, 3,4-dihydro- (7ci,8ci)
isocaramidine
debrisochinum
debrisoquine
debrisoquin
3,4-dihydro-2(1h)-isoquinolinecarboxamidine
2-amidino-1,2,3,4-tetrahydroisoquinoline
3,4-dihydro-2(1h)-isoquinolinecarboximidamide
2(1h)-isoquinolinecarboximidamide, 3,4-dihydro-
DB04840
debrisoquinum [inn-latin]
debrisoquina [inn-spanish]
debrisoquine [inn:ban]
einecs 214-470-1
PRESTWICK0_000372
SPBIO_002444
PRESTWICK1_000372
NCGC00016513-03
NCGC00016513-02
STK232096
HMS2089P09
AKOS000225362
bdbm50122613
FT-0691983
CHEMBL169901 ,
3,4-dihydro-1h-isoquinoline-2-carboximidamide
unii-x31cdk040e
x31cdk040e ,
2(1h)-isoquinolinecarboximidamide,3,4-dihydro-
debrisoquin-13c,15n2 hemisulfate
debrisoquin [mi]
debrisoquine [who-dd]
debrisoquine [inn]
SCHEMBL309184
3,4-dihydro-2(1h)-isoquinolinecarboximidamide #
1,2,3,4-tetrahydroisoquinoline-2-carboximidamide
BS-3952
debrisoquine; isocaramidine
DTXSID7022885
sr-01000075159
SR-01000075159-4
SR-01000075159-1
SBI-0206944.P001
BCP18785
Q3704421
1246814-89-0
SDCCGSBI-0206944.P002
EN300-8045934
HY-B1624
CS-0013557

Research Excerpts

Overview

Debrisoquine is an antihypertensive drug that is metabolized by cytochrome P4502D6. The debrisoquine-test appears to be a useful clinical tool for detecting in patients a genetic deficiency in the hydroxylation of AT-type drugs.

ExcerptReferenceRelevance
"Debrisoquine is a probe drug for in vivo phenotyping of human CYP2D6 metabolic activity. "( The prototypic pharmacogenetic drug debrisoquine is a substrate of the genetically polymorphic organic cation transporter OCT1.
Brockmöller, J; Saadatmand, AR; Tadjerpisheh, S; Tzvetkov, MV, 2012
)
2.1
"Debrisoquine is a major prototypic in-vivo probe used to assess polymorphic CYP2D6 activity in humans, based on the 0-8 h urinary excretion of unchanged drug and its 4-hydroxy metabolite (the so-called metabolic ratio). "( Disposition of debrisoquine in Caucasians with different CYP2D6-genotypes including those with multiple genes.
Bertilsson, L; Dahl, ML; Dalén, P; Eichelbaum, M; Wilkinson, GR, 1999
)
2.1
"Debrisoquine is a substrate of CYP2D6."( Interaction of plasma proteins with cytochromes P450 mediated metabolic reactions: inhibition by human serum albumin and alpha-globulins of the debrisoquine 4-hydroxylation (CYP2D) in liver microsomes of human, hamster and rat.
Ding, LR; Fischer, NE; Inaba, T; Ishii, M; Xu, BQ, 2001
)
1.23
"Debrisoquine is an antihypertensive drug that is metabolized by cytochrome P4502D6. "( The debrisoquine metabolic phenotype and DNA-based assays: implications of misclassification for the association of lung cancer and the debrisoquine metabolic phenotype.
Caporaso, NE; Harris, CC; Hoover, R; Landi, MT; Shaw, GL; Shields, PG; Sugimura, H; Tucker, MA; Weston, A, 1992
)
2.28
"The debrisoquine polymorphism is a common genetic defect that results in deficient oxidation of debrisoquine and numerous other drugs. "( The human CYP2D locus associated with a common genetic defect in drug oxidation: a G1934----A base change in intron 3 of a mutant CYP2D6 allele results in an aberrant 3' splice recognition site.
Gonzalez, FJ; Hanioka, N; Kimura, S; Meyer, UA, 1990
)
0.84
"Debrisoquine is an antihypertensive drug that displays polymorphic metabolism and has been used to determine hydroxylator status in human subjects. "( Improved selectivity of a high-performance liquid chromatography assay for debrisoquine and its 4-hydroxy metabolite from urine.
Johnson, KA; Kolatkar, V; Straka, RJ, 1990
)
1.95
"Debrisoquin is a drug that suppresses the peripheral formation of homovanillic acid without affecting the central formation."( Effects of debrisoquin and haloperidol on plasma homovanillic acid concentration in schizophrenic patients.
Davidson, M; Davis, BM; Davis, KL; Freed, LB; Lesser, JC; Losonczy, MF; Mohs, RC; Mykytyn, VV; Powchik, P, 1987
)
1.38
"The debrisoquine-test appears to be a useful clinical tool for detecting in patients a genetic deficiency in the hydroxylation of AT-type drugs."( Amitriptyline pharmacokinetics and clinical response: II. Metabolic polymorphism assessed by hydroxylation of debrisoquine and mephenytoin.
Baumann, P; Jonzier-Perey, M; Koeb, L; Küpfer, A; Schöpf, J; Tinguely, D, 1986
)
0.96

Effects

Debrisoquine (DQ) has no chiral centre, but hydroxylation in position 4 leads to formation of an asymmetric carbon centre. Debrisoquin has been used to diminish peripheral formation of dopamine to enhance the value of plasma HVA as an index of brain dopaminergic activity.

ExcerptReferenceRelevance
"Debrisoquine polymorphism has been studied extensively in Caucasian populations. "( Evidence for the polymorphic oxidation of debrisoquine in the Thai population.
Lee, EJ; Patamasucon, P; Wanwimolruk, S, 1990
)
1.99
"Debrisoquine phenotyping has potential for identifying carcinogen-exposed workers at high risk of lung cancer."( Lung cancer risk, occupational exposure, and the debrisoquine metabolic phenotype.
Ayesh, R; Caporaso, N; Dosemeci, M; Hayes, RB; Hetzel, M; Hoover, R; Idle, J, 1989
)
1.25
"Debrisoquin has been used to diminish peripheral formation of dopamine to enhance the value of plasma HVA as an index of brain dopaminergic activity."( Assessment of brain dopamine metabolism from plasma HVA and MHPG during debrisoquin treatment: validation in monkeys treated with MPTP.
Bankiewicz, KS; Harvey-White, J; Kopin, IJ, 1988
)
1.23
"Debrisoquine (DQ) has no chiral centre, but hydroxylation in position 4 leads to formation of an asymmetric carbon centre with two possible enantiomers, their absolute configuration being R(-) and S(+)-4-hydroxydebrisoquine (4-OHDQ). "( Enantioselectivity of 4-hydroxylation in extensive and poor metabolizers of debrisoquine.
Bertilsson, L; Eichelbaum, M; Küpfer, A; Meese, CO; Steiner, E, 1988
)
1.95

Treatment

Debrisoquine treatment caused a significant (P less than 0.01) decrease in circulating norepinephrine (-45%) but did not modify plasma levels of angiotensin II, renin, aldosterone, or epinephrine. Debrisoquin pretreatment did not alter the haloperidol-induced increase in plasma HVA.

ExcerptReferenceRelevance
"Debrisoquine treatment caused a significant (P less than 0.01) decrease in circulating norepinephrine (-45%), but did not modify plasma levels of angiotensin II, renin, aldosterone, or epinephrine or the metabolism of sodium or potassium."( Relationship between plasma aldosterone and angiotensin II before and after noradrenergic inhibition in normal subjects and patients with mild essential hypertension.
Beretta-Piccoli, C; Bianchetti, MG; Boehringer, K; Link, L; Morton, JJ; Weidmann, P, 1984
)
0.99
"Debrisoquin pretreatment did not alter the haloperidol-induced increase in plasma HVA and domperidone had no effect on plasma HVA."( Brain contribution to the haloperidol-induced increase in plasma homovanillic acid.
Heninger, GR; Kendler, KS; Roth, RH, 1981
)
0.98
"Pretreatment with debrisoquin did not significantly alter the decrement in plasma HVA produced by apomorphine indicating that a substantial portion of the plasma HVA response to apomorphine is due to the drug's action on brain."( Influence of dopamine agonists on plasma and brain levels of homovanillic acid.
Heninger, GR; Kendler, KS; Roth, RH, 1982
)
0.59
"Pre-treatment with debrisoquine (0.5 mM), reduced the contractions in response to fenfluramine over a period of time."( The sympathomimetic activity of fenfluramine hydrochloride on rat vas deferens.
Mottram, DR; Wadhwani, D, 1977
)
0.58

Toxicity

ExcerptReferenceRelevance
" Other reported effects are toxic confusional states and psychotic reactions."( Psychiatric side effects of antihypertensive drugs other than reserpine.
Fleminger, R; Paykel, ES; Watson, JP, 1982
)
0.26
" However, possession of the CYP2C19*2 allele appears to contribute to adverse cardiac reactions to terodiline."( CYP2D6 and CYP2C19 genotypes of patients with terodiline cardiotoxicity identified through the yellow card system.
Daly, AK; Ford, GA; Wood, SM, 2000
)
0.31

Pharmacokinetics

The primary objectives of the present study were to establish whether there was a pharmacokinetic or pharmacodynamic interaction between the probe drugs caffeine, tolbutamide, debrisoquine and chlorzoxazone.

ExcerptReferenceRelevance
" By using pharmacokinetic pharmacodynamic modeling the pharmacodynamics of racemic metoprolol and the active S-isomer, were quantitated in EMs and PMs in terms of IC50 values, representing metoprolol plasma concentrations resulting in half-maximum receptor occupancy."( Debrisoquine phenotype and the pharmacokinetics and beta-2 receptor pharmacodynamics of metoprolol and its enantiomers.
Jonkers, RE; Koopmans, RP; Portier, EJ; van Boxtel, CJ, 1991
)
1.72
" Mean values of Cmax (445 nmol l-1) and AUC (1660 nmol l-1 h) of codeine in the Chinese were significantly higher than those in the Caucasians (292 nmol l-1 and 1010 nmol l-1 h)."( A comparison of the pharmacokinetics of codeine and its metabolites in healthy Chinese and Caucasian extensive hydroxylators of debrisoquine.
Säwe, J; Sjöqvist, F; Svensson, JO; Yue, QY, 1991
)
0.49
" The mean elimination half-life of quinine in the PMs (10."( Lack of relationship between debrisoquine oxidation phenotype and the pharmacokinetics of quinine.
Chalcroft, S; Wanwimolruk, S, 1991
)
0.57
" Although there was a wide variability in the pharmacokinetic parameters observed, no consistent relationship was found between these and debrisoquine phenotype."( Comparison of the pharmacokinetics of moclobemide in poor and efficient metabolizers of debrisoquine.
Blouin, RA; Guentert, TW; Pfefen, JP; Schoerlin, MP, 1990
)
0.7
" The concentration profile in serum and the pharmacokinetic parameters of the parent drug were similar in both groups."( The relationship between debrisoquine oxidation phenotype and the pharmacokinetics of chlorpropamide.
Huupponen, R; Kallio, J; Pyykkö, K, 1990
)
0.58
"Because both quinidine and propranolol bind to the cytochrome P-450 responsible for the oxidation of debrisoquin, six healthy male subjects were studied to determine whether an interaction occurred between the two drugs and the pharmacodynamic consequences of that interaction."( Quinidine reduces clearance of (+)-propranolol more than (-)-propranolol through marked reduction in 4-hydroxylation.
Anthony, LB; Roden, DM; Wood, AJ; Zhou, HH, 1990
)
0.49
" The poor metaboliser phenotype is associated with increased plasma drug concentrations, a prolongation of elimination half-life and more intense and sustained beta-blockade."( The polymorphic oxidation of beta-adrenoceptor antagonists. Clinical pharmacokinetic considerations.
Lennard, MS; Tucker, GT; Woods, HF,
)
0.13
" No significant differences between the two phenotypes were observed in either the area under the plasma prazosin concentration-time curve, the terminal half-life or the first-dose effect of prazosin."( Lack of relationship between debrisoquine oxidation phenotype and the pharmacokinetics and first dose effect of prazosin.
Lennard, MS; McGourty, JC; Silas, JH, 1988
)
0.57
" In PM subjects, mean values of Cmax (158 ng/ml) and AUC(0-24) (2556 ng X h X m-1) for indoramin were substantially elevated and t 1/2 beta (18."( The pharmacokinetics of indoramin and 6-hydroxyindoramin in poor and extensive hydroxylators of debrisoquine.
Franklin, RA; Pierce, DM; Smith, SE, 1987
)
0.49
" EMs were characterized by a shorter propafenone elimination half-life (5."( Polymorphism of propafenone metabolism and disposition in man: clinical and pharmacokinetic consequences.
McAllister, CB; Roden, DM; Siddoway, LA; Thompson, KA; Wang, T; Wilkinson, GR; Woosley, RL, 1987
)
0.27
"Antipyrine salivary clearance and half-life and the rate of formation of three principal metabolites of antipyrine (4-hydroxyantipyrine, 3-hydroxymethylantipyrine and norantipyrine) were assessed in nine children with congenital adrenal hyperplasia, six of whom were salt-losers and three of whom were non-salt-losers."( Antipyrine clearance and metabolite formation in children with congenital adrenal hyperplasia.
Breimer, DD; Bruining, GJ; De Jongh, BM; Tenkate-Westerhof, EW; Teunissen, MW, 1985
)
0.27
" In this respect, slow EM individuals generally presented intermediate values of those pharmacokinetic parameters."( Influence of debrisoquine hydroxylation phenotype on the pharmacokinetics of mexiletine.
Abrams, SM; Johnston, A; Lledó, P; Patel, M; Pearson, RM; Turner, P, 1993
)
0.66
" Blood and urine samples were collected for pharmacokinetic analyses."( Effect of diprafenone on the pharmacokinetics of digoxin.
Alken, RG; Koytchev, R; Mayer, O, 1996
)
0.29
"To determine whether cytochrome P450 2D6 (CYP2D6) is involved in the metabolism of tolterodine by investigating potential differences in pharmacokinetics and pharmacodynamic (heart rate, accommodation, and salivation) of tolterodine and its 5-hydroxymethyl metabolite between poor metabolizers and extensive metabolizers of debrisoquin (INN, debrisoquine)."( Influence of CYP2D6 polymorphism on the pharmacokinetics and pharmacodynamic of tolterodine.
Alván, G; Bertilsson, L; Brynne, N; Dalén, P; Gabrielsson, J, 1998
)
0.47
" The pharmacokinetics of tolterodine and 5-hydroxymethyl metabolite were determined, and the pharmacodynamic were measured."( Influence of CYP2D6 polymorphism on the pharmacokinetics and pharmacodynamic of tolterodine.
Alván, G; Bertilsson, L; Brynne, N; Dalén, P; Gabrielsson, J, 1998
)
0.3
"The pharmacokinetic parameters in the present study were grossly similar to those found in a study of bambuterol in subjects with normal plasma cholinesterase activity (N)."( Pharmacokinetics of bambuterol in subjects homozygous for the atypical gene for plasma cholinesterase.
Bang, U; Nyberg, L; Rosenborg, J; Viby-Mogensen, J, 1998
)
0.3
" At the end of each study week, the steady-state pharmacokinetic parameters of nortriptyline or paroxetine were determined within the dose interval."( Inhibition of cytochrome P4502D6 activity with paroxetine normalizes the ultrarapid metabolizer phenotype as measured by nortriptyline pharmacokinetics and the debrisoquin test.
Andersson, K; Bertilsson, L; Härtter, S; Laine, K; Svensson, JO; Tybring, G; Widén, J, 2001
)
0.51
"The primary objectives of the present study were to establish whether there was a pharmacokinetic or pharmacodynamic interaction between the probe drugs caffeine (CYP1A2), tolbutamide (CYP2C9), debrisoquine (CYP2D6), chlorzoxazone (CYP2E1) and midazolam (CYP3A4), when administered in combination as a cocktail."( Pharmacokinetic and pharmacodynamic assessment of a five-probe metabolic cocktail for CYPs 1A2, 3A4, 2C9, 2D6 and 2E1.
Aherne, Z; Blakey, GE; Lockton, JA; Norwood, P; Perrett, J; Plume, J; Russell, M, 2004
)
0.51
" Blood pressure and blood glucose measurements were used to assess pharmacodynamic interactions."( Pharmacokinetic and pharmacodynamic assessment of a five-probe metabolic cocktail for CYPs 1A2, 3A4, 2C9, 2D6 and 2E1.
Aherne, Z; Blakey, GE; Lockton, JA; Norwood, P; Perrett, J; Plume, J; Russell, M, 2004
)
0.32
"The five probe drugs when coadministered, in this dosing regimen, demonstrated no evidence of either a metabolic or pharmacodynamic interaction that might confound the conclusions drawn during a cocktail study."( Pharmacokinetic and pharmacodynamic assessment of a five-probe metabolic cocktail for CYPs 1A2, 3A4, 2C9, 2D6 and 2E1.
Aherne, Z; Blakey, GE; Lockton, JA; Norwood, P; Perrett, J; Plume, J; Russell, M, 2004
)
0.32
" The enzymatic activity is reflected by various pharmacokinetic metrics such as the partial clearance of a parent compound to the respective CYP2D6-mediated metabolite or metabolic ratios."( Evaluation of probe drugs and pharmacokinetic metrics for CYP2D6 phenotyping.
Frank, D; Fuhr, U; Jaehde, U, 2007
)
0.34

Bioavailability

ExcerptReferenceRelevance
" The absolute bioavailability after oral administration of 10mg methimazole in the fasting state was high, with a mean of 93%."( Pharmacokinetic properties and bioavailability of methimazole.
Dahlberg, PA; Jansson, R; Lindström, B,
)
0.13
" The variation in plasma morphine concentrations was higher than that of oxycodone, consistent with the lower bioavailability of morphine."( Morphine or oxycodone in cancer pain?
Heiskanen, TE; Kalso, EA; Ruismäki, PM; Seppälä, TA, 2000
)
0.31

Dosage Studied

The ability of normal subjects to hydroxylate mephenytoin (100 mg) or debrisoquine (10 mg) after oral dosing was investigated in 156 unrelated Caucasians living in middle Tennessee. Of the 141 subjects dosed with debrisoquin, 10 proved to be poor oxidizers. There was a significant correlation between the debrisquine to 4-hydroxydebrisoquine ratio and beta-adrenoceptor blockade 24 h after dosing with timolol.

ExcerptRelevanceReference
" Dose-response curves for the pressor effect of norepinephrine were not altered by debrisoquin."( The cardiovascular effects of the antihypertensive drug debrisoquin: a contribution to the pharmacology of chronic treatment. I. One-week administration to dogs.
Cavero, I; Gerold, M; Haeusler, G; Saner, A, 1978
)
0.73
"Where practicable, all subjects found with onset-phase-four blood pressure of 90 mmHg or more after referral were allocated, on a random basis, to alternative antihypertensive regimes at a dosage related to response."( An approach to realistic evaluation of antihypertensive regimes.
Akinkugbe, OO; Basile, U; Carlisle, R; Solagbade, ME, 1977
)
0.26
" In dogs only, seizures appeared within 10-15 min after dosage with minaprine at 20 mg/kg, when the concentrations of minaprine in erythrocytes (6."( Disposition of minaprine in animals and in human extensive and limited debrisoquine hydroxylators.
Berger, Y; Bonnet, JM; Davi, H, 1992
)
0.52
" Three hours after dosing beta-adrenoceptor blocker treatments significantly reduced exercise heart rate, prolonged time to complete exercise, and increased subjective fatigue measured by visual analogue scale."( Influence of debrisoquine oxidation phenotype on exercise tolerance and subjective fatigue after metoprolol and atenolol in healthy subjects.
Jackson, PR; Lennard, MS; Lewis, RV; Ramsay, LE; Tucker, GT; Yeo, WW, 1991
)
0.65
" A comparison between the single and the "cocktail" dosage did not reveal any significant differences in the pharmacokinetic parameters."( [Simultaneous administration of various model substances for characterizing in vivo biotransformation in chronic liver diseases].
Henschel, L; Hoffmann, A; Huster, A; Jorke, D; Kraul, H; Reinhardt, M; Töpfer, R; Truckenbrodt, J, 1990
)
0.28
" The amounts of metoprolol and alpha-hydroxy metoprolol excreted in 0-8 h urine collection, after dosing with 100 mg metoprolol, were measured and the metabolic ratio (% dose excreted as metoprolol/% dose excreted as alpha-hydroxy metoprolol) calculated."( Metoprolol alpha-hydroxylation polymorphism in the San Bushmen of southern Africa.
Avenant, J; Moncrieff, J; Sommers, DK, 1989
)
0.28
" All patients were markedly improved when the daily dosage of the antidepressant was reduced with a simultaneous decrease of the blood concentrations."( High blood concentrations of imipramine or clomipramine and therapeutic failure: a case report study using drug monitoring data.
Balant, LP; Balant-Gorgia, AE; Garrone, G, 1989
)
0.28
" Lewis and Dark Agouti (DA) rat strains (n = 4), models of human extensive and poor metabolizer phenotypes of debrisoquine/sparteine, respectively, were dosed with methoxyphenamine with and without prior administration of quinidine."( Selective in vivo inhibition by quinidine of methoxyphenamine oxidation in rat models of human debrisoquine polymorphism.
Hawes, EM; Inaba, T; McKay, G; Midha, KK; Muralidharan, G, 1989
)
0.71
" If standard doses of beta-blockers are used in poor metabolisers, these subjects may be susceptible to concentration-related adverse reactions and they may also require less frequent dosing for control of angina pectoris."( The polymorphic oxidation of beta-adrenoceptor antagonists. Clinical pharmacokinetic considerations.
Lennard, MS; Tucker, GT; Woods, HF,
)
0.13
" If standard doses of some beta-blockers are used in poor metabolizers, these patients may be susceptible to concentration-related adverse reactions and they may also require lower and less frequent dosing for control of angina pectoris."( Debrisoquine polymorphism and the metabolism and action of metoprolol, timolol, propranolol and atenolol.
Lennard, MS; Silas, JH; Tucker, GT; Woods, HF, 1986
)
1.71
"Optimization of tricyclic antidepressant (TCA) therapy by dosage adjustments made in response to inappropriate concentrations in plasma or side effects can be extremely slow owing to the long half-lives of these drugs."( Is there a practical alternative to therapeutic drug monitoring in therapy with tricyclic antidepressants?
Dawling, S, 1988
)
0.27
" Severe toxicity usually occurs at supratherapeutic plasma levels and might be prevented by tailoring the dosage according to the individual's drug hydroxylating capacity."( Slow hydroxylation of tricyclic antidepressants--relationship to polymorphic drug oxidation.
Bertilsson, L; Sjöqvist, F, 1986
)
0.27
" Vmax and Km were graphically estimated from plasma concentrations at varying phenytoin dosage regimens in 36 of the patients."( The debrisoquin hydroxylation phenotype does not predict the metabolism of phenytoin.
Alván, G; Garle, M; Lind, M; Maguire, JH; McClanahan, JS; Nilson, SO; Sjöqvist, F; Steiner, E; Tomson, T, 1987
)
0.83
" Of the 141 subjects dosed with debrisoquin, 10 proved to be poor oxidizers, and of the 143 subjects dosed with phenformin, 11 were poor oxidizers."( Dissociation of co-regulatory control of debrisoquin/phenformin and sparteine oxidation in Ghanaians.
Eichelbaum, M; Idle, JR; Oates, NS; Smith, RL; Woolhouse, NM, 1985
)
0.82
" In general, there are no pharmacokinetic reasons to adjust dosage in the treatment of thyrotoxicosis, except in the rare case of concomitant advanced hepatic insufficiency."( Pharmacokinetic properties and bioavailability of methimazole.
Dahlberg, PA; Jansson, R; Lindström, B,
)
0.13
" It is concluded that for the majority of patients metoprolol should be prescribed twice daily when using currently available dosage forms."( Polymorphic metabolism of metoprolol: clinical studies.
Lennard, MS; McGourty, JC; Silas, JH; Tucker, GT; Woods, HF, 1985
)
0.27
"The ability of normal subjects to hydroxylate mephenytoin (100 mg) or debrisoquine (10 mg) after oral dosing was investigated in 156 unrelated Caucasians living in middle Tennessee."( Mephenytoin hydroxylation deficiency in Caucasians: frequency of a new oxidative drug metabolism polymorphism.
Aslanian, WS; Branch, RA; McAllister, CB; Wedlund, PJ; Wilkinson, GR, 1984
)
0.5
" 4 In comparison to conventional metoprolol only metoprolol SA was associated with significantly higher plasma metoprolol concentrations at the end of a dosing interval (mean values: conventional, 25 ng/ml, SR 37 ng/ml, SA 51 ng/ml)."( Comparison of two long-acting preparations of metoprolol with conventional metoprolol and atenolol in healthy men during chronic dosing.
Freestone, S; Lennard, MS; Ramsay, LE; Silas, JH, 1982
)
0.26
" Only minor differences in pharmacodynamic effects after tolterodine dosage were observed between the groups."( Influence of CYP2D6 polymorphism on the pharmacokinetics and pharmacodynamic of tolterodine.
Alván, G; Bertilsson, L; Brynne, N; Dalén, P; Gabrielsson, J, 1998
)
0.3
" As a consequence, alteration in metabolism of specific drugs cannot be easily predicted or appropriate dosage adjustment recommendations made."( Selective effect of liver disease on the activities of specific metabolizing enzymes: investigation of cytochromes P450 2C19 and 2D6.
Adedoyin, A; Arns, PA; Branch, RA; Richards, WO; Wilkinson, GR, 1998
)
0.3
" They suggest that recommendations for modification in drug dosage in the presence of liver disease should be based on knowledge of the particular enzyme involved in metabolism of the drug."( Selective effect of liver disease on the activities of specific metabolizing enzymes: investigation of cytochromes P450 2C19 and 2D6.
Adedoyin, A; Arns, PA; Branch, RA; Richards, WO; Wilkinson, GR, 1998
)
0.3
" Concentration-related pharmacologic effects would be expected to be similarly affected by gene dosage and it is likely that the same situation also applies to other drugs whose elimination is importantly determined by this enzyme; for example, many antidepressants and neuroleptics, antiarrhythmic agents, beta-adrenoceptor antagonists and opiates."( Disposition of debrisoquine in Caucasians with different CYP2D6-genotypes including those with multiple genes.
Bertilsson, L; Dahl, ML; Dalén, P; Eichelbaum, M; Wilkinson, GR, 1999
)
0.66
"Paroxetine, with a daily dosage from 20 to 40 mg, is an effective tool in normalizing the metabolic status of CYP2D6 ultrarapid metabolizers."( Inhibition of cytochrome P4502D6 activity with paroxetine normalizes the ultrarapid metabolizer phenotype as measured by nortriptyline pharmacokinetics and the debrisoquin test.
Andersson, K; Bertilsson, L; Härtter, S; Laine, K; Svensson, JO; Tybring, G; Widén, J, 2001
)
0.51
" The 2 h plasma concentration ratios from studies 1 and 2 were combined and a pooled analysis performed to compare ratios within each study (to determine the change in ratio when MDZ was dosed with and without chlorzoxazone) and between studies (to determine the consistency of the ratios when MDZ was given either as part of the two six drug cocktails or when given alone and as part of the five drug cocktail)."( An interaction between the cytochrome P450 probe substrates chlorzoxazone (CYP2E1) and midazolam (CYP3A).
Dickins, M; Gibson, A; Palmer, JL; Pleasance, S; Scott, RJ, 2001
)
0.31
" One must consider the effects of thioridazine dosage on CYP2D6, because it may influence the metabolism of concomitant drugs or produce clinically important adverse effects such as cardiotoxicity."( Effect of thioridazine dosage on the debrisoquine hydroxylation phenotype in psychiatric patients with different CYP2D6 genotypes.
Berecz, R; de la Rubia, A; Dorado, P; Fernández-Salguero, P; LLerena, A, 2001
)
0.58
" One EM subject had a very low oral clearance of fluvoxamine after both single and multiple dosing of the drug."( Low daily 10-mg and 20-mg doses of fluvoxamine inhibit the metabolism of both caffeine (cytochrome P4501A2) and omeprazole (cytochrome P4502C19).
Andersson, K; Bertilsson, L; Carrillo, JA; Christensen, M; Dahl, ML; Mihara, K; Ramos, SI; Tybring, G; Yasui-Furokori, N, 2002
)
0.31
"For patients with attention-deficit/hyperactivity disorder who have hepatic impairment, dosage adjustment is recommended."( Effect of hepatic impairment on the pharmacokinetics of atomoxetine and its metabolites.
Chalon, SA; Desager, JP; Desante, KA; Frye, RF; Golnez, JL; Horsmans, Y; Long, AJ; Sauer, JM; Smith, BP; Thomasson, HR; Witcher, J, 2003
)
0.32
" There was no difference in blood pressure and blood glucose concentrations following the cocktail and dosing of the individual probes."( Pharmacokinetic and pharmacodynamic assessment of a five-probe metabolic cocktail for CYPs 1A2, 3A4, 2C9, 2D6 and 2E1.
Aherne, Z; Blakey, GE; Lockton, JA; Norwood, P; Perrett, J; Plume, J; Russell, M, 2004
)
0.32
"The five probe drugs when coadministered, in this dosing regimen, demonstrated no evidence of either a metabolic or pharmacodynamic interaction that might confound the conclusions drawn during a cocktail study."( Pharmacokinetic and pharmacodynamic assessment of a five-probe metabolic cocktail for CYPs 1A2, 3A4, 2C9, 2D6 and 2E1.
Aherne, Z; Blakey, GE; Lockton, JA; Norwood, P; Perrett, J; Plume, J; Russell, M, 2004
)
0.32
[information is derived through text-mining from research data collected from National Library of Medicine (NLM), extracted Dec-2023]

Roles (4)

RoleDescription
antihypertensive agentAny drug used in the treatment of acute or chronic vascular hypertension regardless of pharmacological mechanism.
adrenergic agentAny agent that acts on an adrenergic receptor or affects the life cycle of an adrenergic transmitter.
sympatholytic agentAny compound which inhibits the postganglionic functioning of the sympathetic nervous system (SNS).
human metaboliteAny mammalian metabolite produced during a metabolic reaction in humans (Homo sapiens).
[role information is derived from Chemical Entities of Biological Interest (ChEBI), Hastings J, Owen G, Dekker A, Ennis M, Kale N, Muthukrishnan V, Turner S, Swainston N, Mendes P, Steinbeck C. (2016). ChEBI in 2016: Improved services and an expanding collection of metabolites. Nucleic Acids Res]

Drug Classes (2)

ClassDescription
isoquinolinesA class of organic heteropolycyclic compound consisting of isoquinoline and its substitution derivatives.
carboxamidineCompounds having the structure RC(=NR)NR2. The term is used as a suffix in systematic nomenclature to denote the -C(=NH)NH2 group including its carbon atom.
[compound class information is derived from Chemical Entities of Biological Interest (ChEBI), Hastings J, Owen G, Dekker A, Ennis M, Kale N, Muthukrishnan V, Turner S, Swainston N, Mendes P, Steinbeck C. (2016). ChEBI in 2016: Improved services and an expanding collection of metabolites. Nucleic Acids Res]

Pathways (6)

PathwayProteinsCompounds
Metabolism14961108
Biological oxidations150276
Phase I - Functionalization of compounds69175
Cytochrome P450 - arranged by substrate type30110
Xenobiotics450
Renz2020 - GEM of Human alveolar macrophage with SARS-CoV-20490

Protein Targets (6)

Inhibition Measurements

ProteinTaxonomyMeasurementAverageMin (ref.)Avg (ref.)Max (ref.)Bioassay(s)
Bile salt export pumpHomo sapiens (human)IC50 (µMol)951.80000.11007.190310.0000AID1449628
Cytochrome P450 2D26Rattus norvegicus (Norway rat)IC50 (µMol)107.00000.09402.16285.6000AID54564
Cytochrome P450 2D6Homo sapiens (human)IC50 (µMol)65.40000.00002.015110.0000AID54564; AID54570
Cytochrome P450 2D4Rattus norvegicus (Norway rat)IC50 (µMol)747.00001.70001.70001.7000AID54566
[prepared from compound, protein, and bioassay information from National Library of Medicine (NLM), extracted Dec-2023]

Biological Processes (37)

Processvia Protein(s)Taxonomy
fatty acid metabolic processBile salt export pumpHomo sapiens (human)
bile acid biosynthetic processBile salt export pumpHomo sapiens (human)
xenobiotic metabolic processBile salt export pumpHomo sapiens (human)
xenobiotic transmembrane transportBile salt export pumpHomo sapiens (human)
response to oxidative stressBile salt export pumpHomo sapiens (human)
bile acid metabolic processBile salt export pumpHomo sapiens (human)
response to organic cyclic compoundBile salt export pumpHomo sapiens (human)
bile acid and bile salt transportBile salt export pumpHomo sapiens (human)
canalicular bile acid transportBile salt export pumpHomo sapiens (human)
protein ubiquitinationBile salt export pumpHomo sapiens (human)
regulation of fatty acid beta-oxidationBile salt export pumpHomo sapiens (human)
carbohydrate transmembrane transportBile salt export pumpHomo sapiens (human)
bile acid signaling pathwayBile salt export pumpHomo sapiens (human)
cholesterol homeostasisBile salt export pumpHomo sapiens (human)
response to estrogenBile salt export pumpHomo sapiens (human)
response to ethanolBile salt export pumpHomo sapiens (human)
xenobiotic export from cellBile salt export pumpHomo sapiens (human)
lipid homeostasisBile salt export pumpHomo sapiens (human)
phospholipid homeostasisBile salt export pumpHomo sapiens (human)
positive regulation of bile acid secretionBile salt export pumpHomo sapiens (human)
regulation of bile acid metabolic processBile salt export pumpHomo sapiens (human)
transmembrane transportBile salt export pumpHomo sapiens (human)
xenobiotic metabolic processCytochrome P450 2D6Homo sapiens (human)
steroid metabolic processCytochrome P450 2D6Homo sapiens (human)
cholesterol metabolic processCytochrome P450 2D6Homo sapiens (human)
estrogen metabolic processCytochrome P450 2D6Homo sapiens (human)
coumarin metabolic processCytochrome P450 2D6Homo sapiens (human)
alkaloid metabolic processCytochrome P450 2D6Homo sapiens (human)
alkaloid catabolic processCytochrome P450 2D6Homo sapiens (human)
monoterpenoid metabolic processCytochrome P450 2D6Homo sapiens (human)
isoquinoline alkaloid metabolic processCytochrome P450 2D6Homo sapiens (human)
xenobiotic catabolic processCytochrome P450 2D6Homo sapiens (human)
retinol metabolic processCytochrome P450 2D6Homo sapiens (human)
long-chain fatty acid biosynthetic processCytochrome P450 2D6Homo sapiens (human)
negative regulation of bindingCytochrome P450 2D6Homo sapiens (human)
oxidative demethylationCytochrome P450 2D6Homo sapiens (human)
negative regulation of cellular organofluorine metabolic processCytochrome P450 2D6Homo sapiens (human)
arachidonic acid metabolic processCytochrome P450 2D6Homo sapiens (human)
[Information is prepared from geneontology information from the June-17-2024 release]

Molecular Functions (16)

Processvia Protein(s)Taxonomy
protein bindingBile salt export pumpHomo sapiens (human)
ATP bindingBile salt export pumpHomo sapiens (human)
ABC-type xenobiotic transporter activityBile salt export pumpHomo sapiens (human)
bile acid transmembrane transporter activityBile salt export pumpHomo sapiens (human)
canalicular bile acid transmembrane transporter activityBile salt export pumpHomo sapiens (human)
carbohydrate transmembrane transporter activityBile salt export pumpHomo sapiens (human)
ABC-type bile acid transporter activityBile salt export pumpHomo sapiens (human)
ATP hydrolysis activityBile salt export pumpHomo sapiens (human)
monooxygenase activityCytochrome P450 2D6Homo sapiens (human)
iron ion bindingCytochrome P450 2D6Homo sapiens (human)
oxidoreductase activityCytochrome P450 2D6Homo sapiens (human)
oxidoreductase activity, acting on paired donors, with incorporation or reduction of molecular oxygen, reduced flavin or flavoprotein as one donor, and incorporation of one atom of oxygenCytochrome P450 2D6Homo sapiens (human)
heme bindingCytochrome P450 2D6Homo sapiens (human)
anandamide 8,9 epoxidase activityCytochrome P450 2D6Homo sapiens (human)
anandamide 11,12 epoxidase activityCytochrome P450 2D6Homo sapiens (human)
anandamide 14,15 epoxidase activityCytochrome P450 2D6Homo sapiens (human)
[Information is prepared from geneontology information from the June-17-2024 release]

Ceullar Components (17)

Processvia Protein(s)Taxonomy
basolateral plasma membraneBile salt export pumpHomo sapiens (human)
Golgi membraneBile salt export pumpHomo sapiens (human)
endosomeBile salt export pumpHomo sapiens (human)
plasma membraneBile salt export pumpHomo sapiens (human)
cell surfaceBile salt export pumpHomo sapiens (human)
apical plasma membraneBile salt export pumpHomo sapiens (human)
intercellular canaliculusBile salt export pumpHomo sapiens (human)
intracellular canaliculusBile salt export pumpHomo sapiens (human)
recycling endosomeBile salt export pumpHomo sapiens (human)
recycling endosome membraneBile salt export pumpHomo sapiens (human)
extracellular exosomeBile salt export pumpHomo sapiens (human)
membraneBile salt export pumpHomo sapiens (human)
mitochondrionCytochrome P450 2D6Homo sapiens (human)
endoplasmic reticulumCytochrome P450 2D6Homo sapiens (human)
endoplasmic reticulum membraneCytochrome P450 2D6Homo sapiens (human)
cytoplasmCytochrome P450 2D6Homo sapiens (human)
intracellular membrane-bounded organelleCytochrome P450 2D6Homo sapiens (human)
[Information is prepared from geneontology information from the June-17-2024 release]

Bioassays (32)

Assay IDTitleYearJournalArticle
AID504749qHTS profiling for inhibitors of Plasmodium falciparum proliferation2011Science (New York, N.Y.), Aug-05, Volume: 333, Issue:6043
Chemical genomic profiling for antimalarial therapies, response signatures, and molecular targets.
AID496831Antimicrobial activity against Cryptosporidium parvum2010Bioorganic & medicinal chemistry, Mar-15, Volume: 18, Issue:6
Multi-target spectral moment QSAR versus ANN for antiparasitic drugs against different parasite species.
AID1449628Inhibition of human BSEP expressed in baculovirus transfected fall armyworm Sf21 cell membranes vesicles assessed as reduction in ATP-dependent [3H]-taurocholate transport into vesicles incubated for 5 mins by Topcount based rapid filtration method2012Drug metabolism and disposition: the biological fate of chemicals, Dec, Volume: 40, Issue:12
Mitigating the inhibition of human bile salt export pump by drugs: opportunities provided by physicochemical property modulation, in silico modeling, and structural modification.
AID496832Antimicrobial activity against Trypanosoma brucei rhodesiense2010Bioorganic & medicinal chemistry, Mar-15, Volume: 18, Issue:6
Multi-target spectral moment QSAR versus ANN for antiparasitic drugs against different parasite species.
AID497005Antimicrobial activity against Pneumocystis carinii2010Bioorganic & medicinal chemistry, Mar-15, Volume: 18, Issue:6
Multi-target spectral moment QSAR versus ANN for antiparasitic drugs against different parasite species.
AID496826Antimicrobial activity against Entamoeba histolytica2010Bioorganic & medicinal chemistry, Mar-15, Volume: 18, Issue:6
Multi-target spectral moment QSAR versus ANN for antiparasitic drugs against different parasite species.
AID352980Antiobesity activity in lean normal BALB/c mouse assessed as change in average daily weight at equimolar dose of 0.5 mmol/kg galegine administered daily through diet for 7 days2009Journal of medicinal chemistry, Jun-11, Volume: 52, Issue:11
Benzylguanidines and other galegine analogues inducing weight loss in mice.
AID496819Antimicrobial activity against Plasmodium falciparum2010Bioorganic & medicinal chemistry, Mar-15, Volume: 18, Issue:6
Multi-target spectral moment QSAR versus ANN for antiparasitic drugs against different parasite species.
AID352982Hypoglycemic activity in lean normal BALB/c mouse assessed as blood glucose level at equimolar dose of 0.5 mmol/kg galegine administered daily through diet for 7 days2009Journal of medicinal chemistry, Jun-11, Volume: 52, Issue:11
Benzylguanidines and other galegine analogues inducing weight loss in mice.
AID496823Antimicrobial activity against Trichomonas vaginalis2010Bioorganic & medicinal chemistry, Mar-15, Volume: 18, Issue:6
Multi-target spectral moment QSAR versus ANN for antiparasitic drugs against different parasite species.
AID678835TP_TRANSPORTER: transepithelial transport (basal to apical) in MDR1-expressing LLC-PK1 cells1999Pharmaceutical research, Mar, Volume: 16, Issue:3
Interrelationship between substrates and inhibitors of human CYP3A and P-glycoprotein.
AID496818Antimicrobial activity against Trypanosoma brucei brucei2010Bioorganic & medicinal chemistry, Mar-15, Volume: 18, Issue:6
Multi-target spectral moment QSAR versus ANN for antiparasitic drugs against different parasite species.
AID496827Antimicrobial activity against Leishmania amazonensis2010Bioorganic & medicinal chemistry, Mar-15, Volume: 18, Issue:6
Multi-target spectral moment QSAR versus ANN for antiparasitic drugs against different parasite species.
AID54562Inhibition of MAMC O-dealkylation mediated by rat Cytochrome P450 2D1 expressed in Saccharomyces cerevisiae2003Journal of medicinal chemistry, Jan-02, Volume: 46, Issue:1
Homology modeling of rat and human cytochrome P450 2D (CYP2D) isoforms and computational rationalization of experimental ligand-binding specificities.
AID352983Antidiabetic activity in lean normal BALB/c mouse assessed as effect on blood lactate level at equimolar dose of 0.5 mmol/kg galegine administered daily through diet for 7 days2009Journal of medicinal chemistry, Jun-11, Volume: 52, Issue:11
Benzylguanidines and other galegine analogues inducing weight loss in mice.
AID54564Inhibition of MAMC O-dealkylation mediated by rat Cytochrome P450 2D2 expressed in Saccharomyces cerevisiae2003Journal of medicinal chemistry, Jan-02, Volume: 46, Issue:1
Homology modeling of rat and human cytochrome P450 2D (CYP2D) isoforms and computational rationalization of experimental ligand-binding specificities.
AID54570Inhibition of MAMC O-dealkylation mediated by human Cytochrome P450 2D6 expressed in human lymphoblastoid cell line2003Journal of medicinal chemistry, Jan-02, Volume: 46, Issue:1
Homology modeling of rat and human cytochrome P450 2D (CYP2D) isoforms and computational rationalization of experimental ligand-binding specificities.
AID496817Antimicrobial activity against Trypanosoma cruzi2010Bioorganic & medicinal chemistry, Mar-15, Volume: 18, Issue:6
Multi-target spectral moment QSAR versus ANN for antiparasitic drugs against different parasite species.
AID496825Antimicrobial activity against Leishmania mexicana2010Bioorganic & medicinal chemistry, Mar-15, Volume: 18, Issue:6
Multi-target spectral moment QSAR versus ANN for antiparasitic drugs against different parasite species.
AID588220Literature-mined public compounds from Kruhlak et al phospholipidosis modelling dataset2008Toxicology mechanisms and methods, , Volume: 18, Issue:2-3
Development of a phospholipidosis database and predictive quantitative structure-activity relationship (QSAR) models.
AID409954Inhibition of mouse brain MAOA2008Journal of medicinal chemistry, Nov-13, Volume: 51, Issue:21
Quantitative structure-activity relationship and complex network approach to monoamine oxidase A and B inhibitors.
AID496829Antimicrobial activity against Leishmania infantum2010Bioorganic & medicinal chemistry, Mar-15, Volume: 18, Issue:6
Multi-target spectral moment QSAR versus ANN for antiparasitic drugs against different parasite species.
AID352981Antiobesity activity in lean normal BALB/c mouse assessed as change in average daily food intake at equimolar dose of 0.5 mmol/kg galegine administered daily through diet for 7 days2009Journal of medicinal chemistry, Jun-11, Volume: 52, Issue:11
Benzylguanidines and other galegine analogues inducing weight loss in mice.
AID496821Antimicrobial activity against Leishmania2010Bioorganic & medicinal chemistry, Mar-15, Volume: 18, Issue:6
Multi-target spectral moment QSAR versus ANN for antiparasitic drugs against different parasite species.
AID54565Inhibition of MAMC O-dealkylation mediated by rat Cytochrome P450 2D3 expressed in Saccharomyces cerevisiae2003Journal of medicinal chemistry, Jan-02, Volume: 46, Issue:1
Homology modeling of rat and human cytochrome P450 2D (CYP2D) isoforms and computational rationalization of experimental ligand-binding specificities.
AID496820Antimicrobial activity against Trypanosoma brucei2010Bioorganic & medicinal chemistry, Mar-15, Volume: 18, Issue:6
Multi-target spectral moment QSAR versus ANN for antiparasitic drugs against different parasite species.
AID496828Antimicrobial activity against Leishmania donovani2010Bioorganic & medicinal chemistry, Mar-15, Volume: 18, Issue:6
Multi-target spectral moment QSAR versus ANN for antiparasitic drugs against different parasite species.
AID496830Antimicrobial activity against Leishmania major2010Bioorganic & medicinal chemistry, Mar-15, Volume: 18, Issue:6
Multi-target spectral moment QSAR versus ANN for antiparasitic drugs against different parasite species.
AID54566Inhibition of MAMC O-dealkylation mediated by rat Cytochrome P450 2D4 expressed in Saccharomyces cerevisiae2003Journal of medicinal chemistry, Jan-02, Volume: 46, Issue:1
Homology modeling of rat and human cytochrome P450 2D (CYP2D) isoforms and computational rationalization of experimental ligand-binding specificities.
AID496824Antimicrobial activity against Toxoplasma gondii2010Bioorganic & medicinal chemistry, Mar-15, Volume: 18, Issue:6
Multi-target spectral moment QSAR versus ANN for antiparasitic drugs against different parasite species.
AID409956Inhibition of mouse brain MAOB2008Journal of medicinal chemistry, Nov-13, Volume: 51, Issue:21
Quantitative structure-activity relationship and complex network approach to monoamine oxidase A and B inhibitors.
AID1159607Screen for inhibitors of RMI FANCM (MM2) intereaction2016Journal of biomolecular screening, Jul, Volume: 21, Issue:6
A High-Throughput Screening Strategy to Identify Protein-Protein Interaction Inhibitors That Block the Fanconi Anemia DNA Repair Pathway.
[information is prepared from bioassay data collected from National Library of Medicine (NLM), extracted Dec-2023]

Research

Studies (842)

TimeframeStudies, This Drug (%)All Drugs %
pre-1990410 (48.69)18.7374
1990's340 (40.38)18.2507
2000's72 (8.55)29.6817
2010's19 (2.26)24.3611
2020's1 (0.12)2.80
[information is prepared from research data collected from National Library of Medicine (NLM), extracted Dec-2023]

Market Indicators

Research Demand Index: 33.96

According to the monthly volume, diversity, and competition of internet searches for this compound, as well the volume and growth of publications, there is estimated to be moderate demand-to-supply ratio for research on this compound.

MetricThis Compound (vs All)
Research Demand Index33.96 (24.57)
Research Supply Index6.89 (2.92)
Research Growth Index4.11 (4.65)
Search Engine Demand Index53.49 (26.88)
Search Engine Supply Index2.00 (0.95)

This Compound (33.96)

All Compounds (24.57)

Study Types

Publication TypeThis drug (%)All Drugs (%)
Trials89 (10.00%)5.53%
Reviews80 (8.99%)6.00%
Case Studies34 (3.82%)4.05%
Observational0 (0.00%)0.25%
Other687 (77.19%)84.16%
[information is prepared from research data collected from National Library of Medicine (NLM), extracted Dec-2023]

Clinical Trials (1)

Trial Overview

TrialPhaseEnrollmentStudy TypeStart DateStatus
Phenotypic and Genotypic Evaluation of Cytochrome P450 Isoforms in Populations of Different Ethnic Composition [NCT00162383]1,200 participants (Anticipated)Interventional1995-07-31Recruiting
[information is prepared from clinicaltrials.gov, extracted Sep-2024]