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Cyclazodone: Difference between revisions
>Scrumptious m Correction of the stated potency, which was in reference to fenozolone (2-monoethylamino), not pemoline, and adjustment of the wording |
>BubatBoy420 m added a "likely" to the unsubstantiated claim that Cyclazodone is a TAAR1 agonist |
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==Pharmacology== | ==Pharmacology== | ||
Cyclazodone is | Cyclazodone is an approximately 3x - 5x more potent N-cyclopropyl derivative of [[pemoline]]. Pemoline is considered to be [[dopamine|dopaminergic]], but its precise method of action has not been fully determined.<ref>"Cylert (Pemoline)" (PDF). FDA. December 2002.</ref> Pemoline has minimal affinity for [[noradrenaline]] receptors and thus has minimal sympathomimetic side effects compared with typical dopaminergic central nervous system stimulants such as methylphenidate and [[Isomer|dextro]]-amphetamine. | ||
According to patents filed by the inventors, cyclazodone exhibited central nervous system stimulating properties and anorexigenic properties more potent than that of pemoline and various other N-lower-alkyl-substituted pemoline derivatives. At the time cyclazodone also offered a much more favorable therapeutic index and margin of safety than pemoline and other N-lower-alkyl-substituted pemoline derivatives.<ref name="GuidicelliPatent">{{Citation | vauthors=((Guidicelli, D. P. R. L.)), ((Najer, H.)) | title=5-phenyl-2-cyclopropylamino-4-oxazolinone, and process for making the same | url=https://patents.google.com/patent/US3609159A/en}}</ref> | According to patents filed by the inventors, cyclazodone exhibited central nervous system stimulating properties and anorexigenic properties more potent than that of pemoline and various other N-lower-alkyl-substituted pemoline derivatives. At the time cyclazodone also offered a much more favorable therapeutic index and margin of safety than pemoline and other N-lower-alkyl-substituted pemoline derivatives.<ref name="GuidicelliPatent">{{Citation | vauthors=((Guidicelli, D. P. R. L.)), ((Najer, H.)) | title=5-phenyl-2-cyclopropylamino-4-oxazolinone, and process for making the same | url=https://patents.google.com/patent/US3609159A/en}}</ref> | ||
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===Pharmacodynamics=== | ===Pharmacodynamics=== | ||
Cyclazodone is an [[amphetamine]]-like [[agonist]] of the Trace Amine Associated Receptor 1 (TAAR1), which is a key regulator of common and trace brain monoamines such as [[dopamine]], [[serotonin]] and [[noradrenaline]].<ref>{{cite journal | vauthors=((Miller, G. M.)) | journal=Journal of neurochemistry | title=The Emerging Role of Trace Amine Associated Receptor 1 in the Functional Regulation of Monoamine Transporters and Dopaminergic Activity | volume=116 | issue=2 | pages=164–176 | date= January 2011 | url=https://www.ncbi.nlm.nih.gov/pmc/articles/PMC3005101/ | issn=0022-3042 | doi=10.1111/j.1471-4159.2010.07109.x}}</ref><ref>{{Citation | title=Amphetamine | url=https://go.drugbank.com/drugs#targets}}</ref><ref>TA1 receptor | http://www.iuphar-db.org/DATABASE/ObjectDisplayForward?objectId=364</ref> The agonism of this set of receptors results in the release of increased concentrations of [[dopamine]], [[serotonin]] and [[noradrenaline]] in the [[synaptic cleft]]. This leads to [[Thought acceleration|cognitive]] and [[Stimulation|physical stimulation]] within the user. | Cyclazodone is likely an [[amphetamine]]-like [[agonist]] of the Trace Amine Associated Receptor 1 (TAAR1), which is a key regulator of common and trace brain monoamines such as [[dopamine]], [[serotonin]] and [[noradrenaline]].<ref>{{cite journal | vauthors=((Miller, G. M.)) | journal=Journal of neurochemistry | title=The Emerging Role of Trace Amine Associated Receptor 1 in the Functional Regulation of Monoamine Transporters and Dopaminergic Activity | volume=116 | issue=2 | pages=164–176 | date= January 2011 | url=https://www.ncbi.nlm.nih.gov/pmc/articles/PMC3005101/ | issn=0022-3042 | doi=10.1111/j.1471-4159.2010.07109.x}}</ref><ref>{{Citation | title=Amphetamine | url=https://go.drugbank.com/drugs#targets}}</ref><ref>TA1 receptor | http://www.iuphar-db.org/DATABASE/ObjectDisplayForward?objectId=364</ref> The agonism of this set of receptors results in the release of increased concentrations of [[dopamine]], [[serotonin]] and [[noradrenaline]] in the [[synaptic cleft]]. This leads to [[Thought acceleration|cognitive]] and [[Stimulation|physical stimulation]] within the user. | ||
==Subjective effects== | ==Subjective effects== | ||
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Another compound related in structure, [[4-methylaminorex]], is associated with pulmonary hypertension<ref>{{cite journal | vauthors=((Gaine, S. P.)), ((Rubin, L. J.)), ((Kmetzo, J. J.)), ((Palevsky, H. I.)), ((Traill, T. A.)) | journal=Chest | title=Recreational use of aminorex and pulmonary hypertension | volume=118 | issue=5 | pages=1496–1497 | date= November 2000 | issn=0012-3692 | doi=10.1378/chest.118.5.1496}}</ref>; though, it is reported to induce far stronger stimulation than that of cyclazodone. | Another compound related in structure, [[4-methylaminorex]], is associated with pulmonary hypertension<ref>{{cite journal | vauthors=((Gaine, S. P.)), ((Rubin, L. J.)), ((Kmetzo, J. J.)), ((Palevsky, H. I.)), ((Traill, T. A.)) | journal=Chest | title=Recreational use of aminorex and pulmonary hypertension | volume=118 | issue=5 | pages=1496–1497 | date= November 2000 | issn=0012-3692 | doi=10.1378/chest.118.5.1496}}</ref>; though, it is reported to induce far stronger stimulation than that of cyclazodone. | ||
The structurally related compound pemoline was | The structurally related compound pemoline was removed from the market after it was found to cause liver damage in children.<ref>{{cite journal | vauthors=((Marotta, P. J.)), ((Roberts, E. A.)) | journal=The Journal of Pediatrics | title=Pemoline hepatotoxicity in children | volume=132 | issue=5 | pages=894–897 | date= May 1998 | url=https://linkinghub.elsevier.com/retrieve/pii/S0022347698703294 | issn=00223476 | doi=10.1016/S0022-3476(98)70329-4}}</ref> | ||
In rodents and primates, sufficiently high doses of monoamine [[releasing agent|releasing agents]] cause dopaminergic neurotoxicity, or damage to dopamine neurons, which is characterized by reduced transporter and receptor function. There is no evidence that [[releasing agent]]s are directly neurotoxic in humans. However, large doses of [[releasing agent]]s may cause indirect neurotoxicity as a result of increased oxidative stress from reactive oxygen species and autoxidation of dopamine.{{citation needed}} | In rodents and primates, sufficiently high doses of monoamine [[releasing agent|releasing agents]] cause dopaminergic neurotoxicity, or damage to dopamine neurons, which is characterized by reduced transporter and receptor function. There is no evidence that [[releasing agent]]s are directly neurotoxic in humans. However, large doses of [[releasing agent]]s may cause indirect neurotoxicity as a result of increased oxidative stress from reactive oxygen species and autoxidation of dopamine.{{citation needed}} | ||