Iprindole

Last updated
Iprindole
Iprindole.svg
Iprindole molecule ball.png
Clinical data
Trade names Prondol, Galatur, Tertran
Other namesPramindole; WY-3263
Routes of
administration 		Oral
ATC code
Legal status
Legal status
  • In general: ℞ (Prescription only)
Pharmacokinetic data
Metabolism Hepatic [1]
Elimination half-life 52.5 hours [2]
Excretion Urine, Feces [3]
Identifiers
  • 3-(6,7,8,9,10,11-hexahydro-5H-cycloocta[b]indol-5-yl)-N,N-dimethylpropan-1-amine
CAS Number
PubChem CID
DrugBank
ChemSpider
UNII
KEGG
ChEBI
ChEMBL
CompTox Dashboard (EPA)
ECHA InfoCard 100.024.485 OOjs UI icon edit-ltr-progressive.svg
Chemical and physical data
Formula C19H28N2
Molar mass 284.447 g·mol−1
3D model (JSmol)
  • c13c(n(c2ccccc12)CCCN(C)C)CCCCCC3
  • InChI=1S/C19H28N2/c1-20(2)14-9-15-21-18-12-6-4-3-5-10-16(18)17-11-7-8-13-19(17)21/h7-8,11,13H,3-6,9-10,12,14-15H2,1-2H3 Yes check.svgY
  • Key:PLIGPBGDXASWPX-UHFFFAOYSA-N Yes check.svgY
   (verify)

Iprindole, sold under the brand names Prondol, Galatur, and Tertran, is an atypical tricyclic antidepressant (TCA) that has been used in the United Kingdom and Ireland for the treatment of depression but appears to no longer be marketed. [4] [5] [6] [7] It was developed by Wyeth and was marketed in 1967. [8] The drug has been described by some as the first "second-generation" antidepressant to be introduced. [9] However, it was very little-used compared to other TCAs, with the number of prescriptions dispensed only in the thousands. [10]

Contents

Medical uses

Iprindole was used in the treatment of major depressive disorder in dosages similar to those of other TCAs. [5] [11]

Contraindications

Iprindole has been associated with jaundice and hepatotoxicity and should not be taken by alcoholics or people with pre-existing liver disease. [8] [12] [13] [14] If such symptoms are encountered iprindole should be discontinued immediately.

Side effects

Anticholinergic side effects such as dry mouth and constipation are either greatly reduced in comparison to imipramine and most other TCAs or fully lacking with iprindole. [15] However, it still has significant antihistamine effects and therefore can produce sedation, though this is diminished relative to other TCAs similarly. [16] Iprindole also lacks significant alpha-blocking properties, and hence does not pose a risk of orthostatic hypotension. [16]

Overdose

In overdose, iprindole is much less toxic than most other TCAs and is considered relatively benign. [17] For instance, between 1974 and 1985, only two deaths associated with iprindole were recorded in the United Kingdom, whereas 278 were reported for imipramine, although imipramine is used far more often than iprindole. [10] [17]

Interactions

Iprindole has been shown to be a potent inhibitor of the aromatic hydroxylation and/or N-dealkylation-mediated metabolism of many substances including, but not limited to octopamine, amphetamine, methamphetamine, fenfluramine, phenelzine, tranylcypromine, trimipramine, and fluoxetine, likely via inactivating cytochrome P450 enzymes. [1] [18] [19] [20] [21] [22] It also inhibits its own metabolism. [21]

On account of these interactions, caution should be used when combining iprindole with other drugs. [1] As an example, when administered with amphetamine or methamphetamine, iprindole increases their brain concentrations and prolongs their terminal half-lives by 2- to 3-fold, strongly augmenting both their physiological effects and neurotoxicity in the process. [23] [24] [25]

Pharmacology

Pharmacodynamics

Iprindole [26]
SiteKi (nM)SpeciesRef
SERT 1,620–3,300Human [27] [28]
NET 1,262Human [27]
DAT 6,530Human [27]
5-HT1A 2,800Human [28]
5-HT2A 217–280Human/rat [28] [29]
5-HT2C 206Rat [29]
α1 2,300Human [30]
α2 8,600Human [30]
β >10,000Mammal [31] [32]
D2 6,300Rat [32]
H1 100–130Human/rat [30] [33]
H2 200–8,300Guinea pig [32] [34] [35]
mACh 2,100Human [30] [36]
σ1 >10,000Rat [37]
Values are Ki (nM). The smaller the value, the more strongly the drug binds to the site.

Iprindole is unique compared to most other TCAs in that it is a very weak and negligible inhibitor of the reuptake of serotonin and norepinephrine and appears to act instead as a selective albeit weak antagonist of 5-HT2 receptors; hence its classification by some as "second-generation". [38] [39] [40] Additionally, iprindole has very weak/negligible antiadrenergic and anticholinergic activity and weak although possibly significant antihistamine activity; as such, side effects of iprindole are much less prominent relative to other TCAs, and it is well tolerated. [15] However, iprindole may not be as effective as other TCAs, particularly in terms of anxiolysis. [38] [16] Based on animal research, the antidepressant effects of iprindole may be mediated through downstream dopaminergic mechanisms. [41]

The binding affinities of iprindole for various biological targets are presented in the table to the right. [26] It is presumed to act as an inhibitor or antagonist/inverse agonist of all sites. Considering the range of its therapeutic concentrations (e.g., 63–271 nM at 90 mg/day), [2] only the actions of iprindole on the 5-HT2 and histamine receptors might be anticipated to be of possible clinical significance. [2] However, it is unknown whether these actions are in fact responsible for the antidepressant effects of iprindole. The plasma protein binding of iprindole and hence its free percentage and potentially bioactive concentrations do not seem to be known.

Pharmacokinetics

Only one study appears to have evaluated the pharmacokinetics of iprindole. [2] [42] A single oral dose of 60 mg iprindole to healthy volunteers has been found to achieve mean peak plasma concentrations of 67.1 ng/mL (236 nmol/L) after 2 to 4 hours. [2] The mean terminal half-life of iprindole was 52.5 hours, which is notably much longer than that of other TCAs like amitriptyline and imipramine. [2] Following chronic treatment with 90 mg/day iprindole for 3 weeks, plasma concentrations of the drug ranged between 18 and 77 ng/mL (63–271 nmol/L). [2] Theoretical steady-state concentrations should be reached by 99% within 15 to 20 days of treatment. [2]

Chemistry

Iprindole is a tricyclic compound, specifically a cyclooctaindole (that is, an indole nucleus joined with a cyclooctyl ring), and possesses three rings fused together with a side chain attached in its chemical structure. [43] It is a tertiary amine TCA, although its ring system and pharmacological properties are very different from those of other TCAs. [15] [44] Other tertiary amine TCAs that are similar to iprindole include butriptyline and trimipramine. [45] [46] The chemical name of iprindole is 3-(6,7,8,9,10,11-hexahydro-5H-cycloocta[b]indol-5-yl)-N,N-dimethylpropan-1-amine and its free base form has a chemical formula of C19H28N2 with a molecular weight of 284.439 g/mol. [47] The drug has been used commercially as both the free base and the hydrochloride salt. [47] The CAS Registry Number of the free base is 5560-72-5 and of the hydrochloride is 20432-64-8. [47]

History

Iprindole was developed by Wyeth and was marketed in 1967. [8] [48]

Society and culture

Generic names

Iprindole is the English and French generic name of the drug and its INN, USAN, BAN, and DCF, while iprindole hydrochloride is its BANM. [47] [4] [49] Its generic name in Spanish and German is iprindol while its generic name in Latin is iprindolum. [4] Iprindole was originally known unofficially as pramindole. [47] [4]

Brand names

Iprindole has been marketed under the brand name Prondol by Wyeth in the United Kingdom and Ireland for the indication of major depressive disorder, [50] and has also been sold as Galatur and Tertran by Wyeth. [47]

Availability

Iprindole was previously available in the United Kingdom and Ireland [50] but seems to no longer be available for medical use in any country. [4]

Related Research Articles

An anxiolytic is a medication or other intervention that reduces anxiety. This effect is in contrast to anxiogenic agents which increase anxiety. Anxiolytic medications are used for the treatment of anxiety disorders and their related psychological and physical symptoms.

<span class="mw-page-title-main">Tricyclic antidepressant</span> Class of medications

Tricyclic antidepressants (TCAs) are a class of medications that are used primarily as antidepressants, which is important for the management of depression. They are second-line drugs next to SSRIs. TCAs were discovered in the early 1950s and were marketed later in the decade. They are named after their chemical structure, which contains three rings of atoms. Tetracyclic antidepressants (TeCAs), which contain four rings of atoms, are a closely related group of antidepressant compounds.

<span class="mw-page-title-main">Maprotiline</span> Antidepressant

Maprotiline, sold under the brand name Ludiomil among others, is a tetracyclic antidepressant (TeCA) that is used in the treatment of depression. It may alternatively be classified as a tricyclic antidepressant (TCA), specifically a secondary amine. In terms of its chemistry and pharmacology, maprotiline is closely related to other secondary amine TCAs like nortriptyline and protriptyline, and has similar effects to them.

<span class="mw-page-title-main">Amitriptyline</span> Tricyclic antidepressant

Amitriptyline, sold under the brand name Elavil among others, is a tricyclic antidepressant primarily used to treat major depressive disorder, a variety of pain syndromes such as neuropathic pain, fibromyalgia, migraine and tension headaches. Due to the frequency and prominence of side effects, amitriptyline is generally considered a second-line therapy for these indications.

<span class="mw-page-title-main">Chlorphenamine</span> Antihistamine used to treat allergies

Chlorphenamine, also known as chlorpheniramine, is an antihistamine used to treat the symptoms of allergic conditions such as allergic rhinitis. It is taken by mouth. The medication takes effect within two hours and lasts for about 4-6 hours.

<span class="mw-page-title-main">Amoxapine</span> Chemical compound

Amoxapine, sold under the brand name Asendin among others, is a tricyclic antidepressant (TCA). It is the N-demethylated metabolite of loxapine. Amoxapine first received marketing approval in the United States in 1992, approximately 30 to 40 years after most of the other TCAs were introduced in the United States.

<span class="mw-page-title-main">Imipramine</span> Antidepressant

Imipramine, sold under the brand name Tofranil, among others, is a tricyclic antidepressant (TCA) mainly used in the treatment of depression. It is also effective in treating anxiety and panic disorder. Imipramine may also be used off-label for nocturnal enuresis and chronic pain. Imipramine is taken by mouth.

<span class="mw-page-title-main">Desipramine</span> Antidepressant

Desipramine, sold under the brand name Norpramin among others, is a tricyclic antidepressant (TCA) used in the treatment of depression. It acts as a relatively selective norepinephrine reuptake inhibitor, though it does also have other activities such as weak serotonin reuptake inhibitory, α1-blocking, antihistamine, and anticholinergic effects. The drug is not considered a first-line treatment for depression since the introduction of selective serotonin reuptake inhibitor (SSRI) antidepressants, which have fewer side effects and are safer in overdose.

<span class="mw-page-title-main">Clomipramine</span> Antidepressant

Clomipramine, sold under the brand name Anafranil among others, is a tricyclic antidepressant (TCA). It is used for the treatment of obsessive–compulsive disorder, panic disorder, major depressive disorder, and chronic pain. It may increase the risk of suicide in those under the age of 25. It is primarily taken by mouth. It has also been used to treat premature ejaculation.

<span class="mw-page-title-main">Nortriptyline</span> Antidepressant medication

Nortriptyline, sold under the brand name Pamelor, among others, is a medication used to treat depression. This medicine is also sometimes used for neuropathic pain, attention deficit hyperactivity disorder (ADHD), smoking cessation and anxiety. As with many antidepressants, its use for young people with depression and other psychiatric disorders may be limited due to increased suicidality in the 18-24 population initiating treatment. Nortriptyline is a less preferred treatment for ADHD and stopping smoking. It is taken by mouth.

<span class="mw-page-title-main">Doxepin</span> Medication to treat depressive disorder, anxiety disorders, chronic hives, and trouble sleeping

Doxepin is a medication belonging to the tricyclic antidepressant (TCA) class of drugs used to treat major depressive disorder, anxiety disorders, chronic hives, and insomnia. For hives it is a less preferred alternative to antihistamines. It has a mild to moderate benefit for sleeping problems. It is used as a cream for itchiness due to atopic dermatitis or lichen simplex chronicus.

<span class="mw-page-title-main">Trimipramine</span> Antidepressant

Trimipramine, sold under the brand name Surmontil among others, is a tricyclic antidepressant (TCA) which is used to treat depression. It has also been used for its sedative, anxiolytic, and weak antipsychotic effects in the treatment of insomnia, anxiety disorders, and psychosis, respectively. The drug is described as an atypical or "second-generation" TCA because, unlike other TCAs, it seems to be a fairly weak monoamine reuptake inhibitor. Similarly to other TCAs however, trimipramine does have antihistamine, antiserotonergic, antiadrenergic, antidopaminergic, and anticholinergic activities. And When heated to decomposition ,it emits toxic fumes of NOx.

<span class="mw-page-title-main">Dosulepin</span> Antidepressant

Dosulepin, also known as dothiepin and sold under the brand name Prothiaden among others, is a tricyclic antidepressant (TCA) which is used in the treatment of depression. Dosulepin was once the most frequently prescribed antidepressant in the United Kingdom, but it is no longer widely used due to its relatively high toxicity in overdose without therapeutic advantages over other TCAs. It acts as a serotonin–norepinephrine reuptake inhibitor (SNRI) and also has other activities including antihistamine, antiadrenergic, antiserotonergic, anticholinergic, and sodium channel-blocking effects.

<span class="mw-page-title-main">Dibenzepin</span> Chemical compound

Dibenzepin, sold under the brand name Noveril among others, is a tricyclic antidepressant (TCA) used widely throughout Europe for the treatment of depression. It has similar efficacy and effects relative to other TCAs like imipramine but with fewer side effects.

<span class="mw-page-title-main">Mianserin</span> Antidepressant

Mianserin, sold under the brand name Tolvon among others, is an atypical antidepressant that is used primarily in the treatment of depression in Europe and elsewhere in the world. It is a tetracyclic antidepressant (TeCA). Mianserin is closely related to mirtazapine, both chemically and in terms of its actions and effects, although there are significant differences between the two drugs.

<span class="mw-page-title-main">Butriptyline</span> Pharmaceutical drug

Butriptyline, sold under the brand name Evadyne among others, is a tricyclic antidepressant (TCA) that has been used in the United Kingdom and several other European countries for the treatment of depression but appears to no longer be marketed. Along with trimipramine, iprindole, and amoxapine, it has been described as an "atypical" or "second-generation" TCA due to its relatively late introduction and atypical pharmacology. It was very little-used compared to other TCAs, with the number of prescriptions dispensed only in the thousands.

<span class="mw-page-title-main">Lofepramine</span> Chemical compound

Lofepramine, sold under the brand names Gamanil, Lomont, and Tymelyt among others, is a tricyclic antidepressant (TCA) which is used to treat depression. The TCAs are so named as they share the common property of having three rings in their chemical structure. Like most TCAs lofepramine is believed to work in relieving depression by increasing concentrations of the neurotransmitters norepinephrine and serotonin in the synapse, by inhibiting their reuptake. It is usually considered a third-generation TCA, as unlike the first- and second-generation TCAs it is relatively safe in overdose and has milder and less frequent side effects.

<span class="mw-page-title-main">Opipramol</span> Drug used to treat depressive and anxiety disorders

Opipramol, sold under the brand name Insidon among others, is an anxiolytic and tricyclic antidepressant that is used throughout Europe. Despite chemically being a tricyclic dibenzazepine (iminostilbene) derivative similar to imipramine, opipramol is not a reuptake inhibitor like most other tricyclic antidepressants, and instead, uniquely among antidepressants, acts primarily as a SIGMAR1 agonist. It was developed by Schindler and Blattner in 1961.

<span class="mw-page-title-main">Amitriptylinoxide</span> Chemical compound

Amitriptylinoxide, or amitriptyline N-oxide, is a tricyclic antidepressant (TCA) which was introduced in Europe in the 1970s for the treatment of depression.

<span class="mw-page-title-main">Imipraminoxide</span> Chemical compound

Imipraminoxide, or imipramine N-oxide, is a tricyclic antidepressant (TCA) that was introduced in Europe in the 1960s for the treatment of depression.

References

  1. 1 2 3 Rotzinger S, Bourin M, Akimoto Y, Coutts RT, Baker GB (August 1999). "Metabolism of some "second"- and "fourth"-generation antidepressants: iprindole, viloxazine, bupropion, mianserin, maprotiline, trazodone, nefazodone, and venlafaxine". Cellular and Molecular Neurobiology. 19 (4): 427–442. doi:10.1023/A:1006953923305. PMID   10379419. S2CID   19585113.
  2. 1 2 3 4 5 6 7 8 Caillé G, de Montigny C, Besner JG (1982). "Quantitation of iprindole in plasma by GLC". Biopharmaceutics & Drug Disposition. 3 (1): 11–17. doi:10.1002/bdd.2510030103. PMID   7082775.
  3. ↑ Sisenwine SF, Tio CO, Ruelius HW (April 1979). "The disposition of [14C]iprindole in man, dog, miniature swine, rhesus monkey and rat". Xenobiotica; the Fate of Foreign Compounds in Biological Systems. 9 (4): 237–246. doi:10.3109/00498257909038726. PMID   113942.
  4. 1 2 3 4 5 Index Nominum 2000: International Drug Directory. Taylor & Francis. 2000. pp. 569–. ISBN   978-3-88763-075-1.
  5. 1 2 Ayd, Frank J. (2000). Lexicon of psychiatry, neurology, and the neurosciences. Philadelphia, Pa: Lippincott-Williams & Wilkins. ISBN   0-7817-2468-6.
  6. ↑ Dictionary of organic compounds. London: Chapman & Hall. 1996. ISBN   0-412-54090-8.
  7. ↑ Davison, Gerald C.; Hooley, Jill M.; Neale, John M. (1989). Readings in abnormal psychology . New York: Wiley. p.  186. ISBN   0-471-63107-8. iprindole.
  8. 1 2 3 "Jaundice from iprindole (Prondol)". Drug and Therapeutics Bulletin. 9 (3): 10–11. January 1971. doi:10.1136/dtb.9.3.10. PMID   5548547. S2CID   31232918.
  9. ↑ Horn AS, Trace RC (January 1983). "Second generation antidepressants: The pharmacological and clinical significance of selected examples". Drug Development Research. 3 (3): 203–211. doi:10.1002/ddr.430030302. S2CID   84018071.
  10. 1 2 J. K. Aronson (2009). Meyler's Side Effects of Psychiatric Drugs. Elsevier. pp. 18–. ISBN   978-0-444-53266-4.
  11. ↑ Wing, Lorna; Wing, J. K. (1982). Psychoses of uncertain aetiology. Cambridge, UK: Cambridge University Press. ISBN   0-521-28438-4.
  12. ↑ Aronson, Jeffrey Kenneth (2008). Meyler's Side Effects of Psychiatric Drugs (Meylers Side Effects). Amsterdam: Elsevier Science. ISBN   978-0-444-53266-4.
  13. ↑ Ajdukiewicz AB, Grainger J, Scheuer PJ, Sherlock S (September 1971). "Jaundice due to iprindole". Gut. 12 (9): 705–708. doi:10.1136/gut.12.9.705. PMC   1411804 . PMID   4106521.
  14. ↑ Clift AD (June 1971). "Allergy to iprindole (Prondole) with hepatotoxicity". British Medical Journal. 2 (5763): 712. doi:10.1136/bmj.2.5763.712. PMC   1796275 . PMID   5556082.
  15. 1 2 3 Gwynn Pennant Ellis; Geoffrey Buckle West (1970). Progress in Medicinal Chemistry: 7. Butterworth-Heinemann. pp. 25–. ISBN   978-0-408-70013-9.
  16. 1 2 3 Rickels K, Chung HR, Csanalosi I, Sablosky L, Simon JH (September 1973). "Iprindole and imipramine in non-psychotic depressed out-patients". The British Journal of Psychiatry. 123 (574): 329–339. doi:10.1192/bjp.123.3.329. PMID   4583430. S2CID   23126539.
  17. 1 2 Cassidy S, Henry J (October 1987). "Fatal toxicity of antidepressant drugs in overdose". British Medical Journal. 295 (6605): 1021–1024. doi:10.1136/bmj.295.6605.1021. PMC   1248068 . PMID   3690249.
  18. ↑ Sedlock ML, Ravitch J, Edwards DJ (August 1985). "The effects of imipramine and iprindole on the metabolism of octopamine in the rat". Neuropharmacology. 24 (8): 705–708. doi:10.1016/0028-3908(85)90002-4. PMID   3939325. S2CID   39933551.
  19. ↑ Hegadoren KM, Baker GB, Coutts RT, Dewhurst WG (March 1991). "Interactions of iprindole with fenfluramine metabolism in rat brain and liver". Journal of Psychiatry & Neuroscience. 16 (1): 5–11. PMC   1188281 . PMID   2049371.
  20. ↑ Yamamoto T, Takano R, Egashira T, Yamanaka Y (November 1984). "Metabolism of methamphetamine, amphetamine and p-hydroxymethamphetamine by rat-liver microsomal preparations in vitro". Xenobiotica; the Fate of Foreign Compounds in Biological Systems. 14 (11): 867–875. doi:10.3109/00498258409151485. PMID   6506759.
  21. 1 2 Coutts RT, Hussain MS, Baker GB (December 1991). "Effect of iprindole on the metabolism of trimipramine in the rat". Journal of Psychiatry & Neuroscience. 16 (5): 272–275. PMC   1188365 . PMID   1797102.
  22. ↑ Aspeslet LJ, Baker GB, Coutts RT, Torok-Both GA (1994). "The effects of desipramine and iprindole on levels of enantiomers of fluoxetine in rat brain and urine". Chirality. 6 (2): 86–90. doi:10.1002/chir.530060208. PMID   8204417.
  23. ↑ Fuller RW, Baker JC, Molloy BB (February 1977). "Biological disposition of rigid analogs of amphetamine". Journal of Pharmaceutical Sciences. 66 (2): 271–272. doi:10.1002/jps.2600660235. PMID   839428.
  24. ↑ Fuller RW, Hemrick-Luecke S (July 1980). "Long-lasting depletion of striatal dopamine by a single injection of amphetamine in iprindole-treated rats". Science. 209 (4453): 305–307. Bibcode:1980Sci...209..305F. doi:10.1126/science.7384808. PMID   7384808.
  25. ↑ Peat MA, Warren PF, Gibb JW (April 1983). "Effects of a single dose of methamphetamine and iprindole on the serotonergic and dopaminergic system of the rat brain". The Journal of Pharmacology and Experimental Therapeutics. 225 (1): 126–131. PMID   6187915.
  26. 1 2 Roth BL, Driscol J. "PDSP Ki Database". Psychoactive Drug Screening Program (PDSP). University of North Carolina at Chapel Hill and the United States National Institute of Mental Health. Retrieved 7 May 2022.
  27. 1 2 3 Tatsumi M, Groshan K, Blakely RD, Richelson E (December 1997). "Pharmacological profile of antidepressants and related compounds at human monoamine transporters". European Journal of Pharmacology. 340 (2–3): 249–258. doi:10.1016/s0014-2999(97)01393-9. PMID   9537821.
  28. 1 2 3 Wander TJ, Nelson A, Okazaki H, Richelson E (December 1986). "Antagonism by antidepressants of serotonin S1 and S2 receptors of normal human brain in vitro". European Journal of Pharmacology. 132 (2–3): 115–121. doi:10.1016/0014-2999(86)90596-0. PMID   3816971.
  29. 1 2 Pälvimäki EP, Roth BL, Majasuo H, Laakso A, Kuoppamäki M, Syvälahti E, Hietala J (August 1996). "Interactions of selective serotonin reuptake inhibitors with the serotonin 5-HT2c receptor". Psychopharmacology. 126 (3): 234–240. doi:10.1007/bf02246453. PMID   8876023. S2CID   24889381.
  30. 1 2 3 4 Richelson E, Nelson A (July 1984). "Antagonism by antidepressants of neurotransmitter receptors of normal human brain in vitro". The Journal of Pharmacology and Experimental Therapeutics. 230 (1): 94–102. PMID   6086881.
  31. ↑ Bylund DB, Snyder SH (July 1976). "Beta adrenergic receptor binding in membrane preparations from mammalian brain". Molecular Pharmacology. 12 (4): 568–580. PMID   8699.
  32. 1 2 3 Baker GB, Greenshaw AJ (1988). "In Vitro and Ex Vivo Neurochemical Screening Procedures for Antidepressants, Neuroleptics, and Benzodiazepines". Analysis of Psychiatric Drugs. Vol. 10. pp. 327–378. doi:10.1385/0-89603-121-7:327. ISBN   0-89603-121-7.
  33. ↑ Tran VT, Chang RS, Snyder SH (December 1978). "Histamine H1 receptors identified in mammalian brain membranes with [3H]mepyramine". Proceedings of the National Academy of Sciences of the United States of America. 75 (12): 6290–6294. Bibcode:1978PNAS...75.6290T. doi: 10.1073/pnas.75.12.6290 . PMC   393167 . PMID   282646.
  34. ↑ Tsai BS, Yellin TO (November 1984). "Differences in the interaction of histamine H2 receptor antagonists and tricyclic antidepressants with adenylate cyclase from guinea pig gastric mucosa". Biochemical Pharmacology. 33 (22): 3621–3625. doi:10.1016/0006-2952(84)90147-3. PMID   6150708.
  35. ↑ Kanba S, Richelson E (October 1983). "Antidepressants are weak competitive antagonists of histamine H2 receptors in dissociated brain tissue". European Journal of Pharmacology. 94 (3–4): 313–318. doi:10.1016/0014-2999(83)90420-x. PMID   6140176.
  36. ↑ El-Fakahany E, Richelson E (January 1983). "Antagonism by antidepressants of muscarinic acetylcholine receptors of human brain". British Journal of Pharmacology. 78 (1): 97–102. doi:10.1111/j.1476-5381.1983.tb17361.x. PMC   2044798 . PMID   6297650.
  37. ↑ Largent BL, Gundlach AL, Snyder SH (August 1984). "Psychotomimetic opiate receptors labeled and visualized with (+)-[3H]3-(3-hydroxyphenyl)-N-(1-propyl)piperidine". Proceedings of the National Academy of Sciences of the United States of America. 81 (15): 4983–4987. Bibcode:1984PNAS...81.4983L. doi: 10.1073/pnas.81.15.4983 . PMC   391617 . PMID   6087359.
  38. 1 2 Zis AP, Goodwin FK (September 1979). "Novel antidepressants and the biogenic amine hypothesis of depression. The case for iprindole and mianserin". Archives of General Psychiatry. 36 (10): 1097–1107. doi:10.1001/archpsyc.1979.01780100067006. PMID   475543.
  39. ↑ Jaramillo J, Greenberg R (February 1975). "Comparative pharmacological studies on butriptyline and some related standard tricyclic antidepressants". Canadian Journal of Physiology and Pharmacology. 53 (1): 104–112. doi:10.1139/y75-014. PMID   166748.
  40. ↑ Horn AS, Trace RC (July 1974). "Structure-activity relations for the inhibition of 5-hydroxytryptamine uptake by tricyclic antidepressants into synaptosomes from serotoninergic neurones in rat brain homogenates". British Journal of Pharmacology. 51 (3): 399–403. doi:10.1111/j.1476-5381.1974.tb10675.x. PMC   1776771 . PMID   4451753.
  41. ↑ Berettera C, Invernizzi R, Pulvirenti L, Samanin R (April 1986). "Chronic treatment with iprindole reduces immobility of rats in the behavioural 'despair' test by activating dopaminergic mechanisms in the brain". The Journal of Pharmacy and Pharmacology. 38 (4): 313–315. doi:10.1111/j.2042-7158.1986.tb04576.x. PMID   2872301. S2CID   27863022.
  42. ↑ Goodnick PJ (October 1994). "Pharmacokinetic optimisation of therapy with newer antidepressants". Clinical Pharmacokinetics. 27 (4): 307–330. doi:10.2165/00003088-199427040-00005. PMID   7834966. S2CID   46783536.
  43. ↑ Yong Zhou (22 October 2013). Drugs in Psychiatric Practice. Elsevier. pp. 195–. ISBN   978-1-4831-9193-5.
  44. ↑ Baxter BL, Gluckman MI (August 1969). "Iprindole: an antidepressant which does not block REM sleep". Nature. 223 (5207): 750–752. Bibcode:1969Natur.223..750B. doi:10.1038/223750a0. PMID   4308422. S2CID   4181062.
  45. ↑ Patricia K. Anthony (2002). Pharmacology Secrets. Elsevier Health Sciences. pp. 39–. ISBN   1-56053-470-2.
  46. ↑ Philip Cowen; Paul Harrison; Tom Burns (9 August 2012). Shorter Oxford Textbook of Psychiatry. OUP Oxford. pp. 532–. ISBN   978-0-19-162675-3.
  47. 1 2 3 4 5 6 J. Elks (14 November 2014). The Dictionary of Drugs: Chemical Data: Chemical Data, Structures and Bibliographies. Springer. pp. 702–. ISBN   978-1-4757-2085-3.
  48. ↑ Richard C. Dart (2004). Medical Toxicology. Lippincott Williams & Wilkins. pp. 836–. ISBN   978-0-7817-2845-4.
  49. ↑ I.K. Morton; Judith M. Hall (6 December 2012). Concise Dictionary of Pharmacological Agents: Properties and Synonyms. Springer Science & Business Media. pp. 156–. ISBN   978-94-011-4439-1.
  50. 1 2 Sean C. Sweetman (2009). Martindale: The Complete Drug Reference, 36th Edition. London: Pharmaceutical Press. ISBN   978-0-85369-840-1.

Further reading

This page is based on this Wikipedia article
Text is available under the CC BY-SA 4.0 license; additional terms may apply.
Images, videos and audio are available under their respective licenses.