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Inibidor de recaptação de serotonina-noradrenalina-dopamina

Origem: Wikipédia, a enciclopédia livre.
(Redirecionado deSNDRI)

Osinibidores de recaptação de serotonina-noradrenalina-dopamina (SNDRIs), também conhecidos comoinibidores triplos de recaptação (TRI), são uma classe farmacológica composta pordrogas que inibem a recaptação dos neurotransmissoresmonoamínicos:serotonina,noradrenalina edopamina.

Seu mecanismo de ação inibe, ao mesmo tempo, arecaptação neuronal dotransportador de serotonina (SERT),noradrenalina (NET) e odopamina (DAT). A inibição da recaptação desses neurotransmissores aumenta suas concentrações extracelulares e, portanto, estimulam a neurotransmissão serotoninérgica, noradrenérgica e dopaminérgica.

Usos clínicos

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Depressão

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Otranstorno depressivo maior (TDM) é uma das principais patologias que sustentam a necessidade de desenvolvimento dos SNDRIs.[1][2][3][4][5][6][7][8][9][10] De acordo com aOrganização Mundial da Saúde (OMS), em 2006 adepressão foi a principal causa dedeficiências e a quarta maior responsável pelaCarga Global de Morbidade (CGM). Estima-se que a depressão atinga a segunda posição no ranking deesperança de vida corrigida pela incapacidade por volta de 2020.[11]

Farmacoterapia

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Os SNDRIs são utilizados quando outros fármacos não produzem os efeitos terapêuticos esperados, como em casos dedepressão resistente a tratamento. Embora dois terços das pessoas respondam adequadamento ao tratamento com outros antidepressivos, um terço das pessoas responde aoplacebo,[12] e a taxa derecidiva (remissão incompleta_ devido aos sintomas de rebote são altas. Além da altaxa taxa de remissão pós-tratamento, os sintomas depressivos podem reaparecer mesmo ao decorrer das terapias de longo prazo (taquifilaxia). Além disso, os antidepressivos disponíveis atualmente provocam efeitos colaterais indesejáveis, de modo que a pesquisa médica busca compostos com menor potencial de efeitos adversos a fim de diminuir as recidivas ou desistências de tratamento.[6]

Outros

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Lista de SNDRIs

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Fármacos aprovados

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SNDRIs fracos

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Ensaios clínicos em andamento

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Ensaios clínicos interrompidos

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  • Bicifadina (DOV-220.075) - interrompido em 1981[37][38]
  • BMS-866.949
  • Brasofensina (NS-2214, BMS-204,756) (1995)[39]
  • Diclofensina (Ro 8-4650) (1982)[40][41]
  • DOV-216.303 (2004)[42][43]
  • EXP-561 (1965)[44]
  • Liafensina (BMS-820.836)
  • NS-2359 (GSK-372.475)[45]
  • RG-7166 (2009–2012)

Drogas projetadas

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Compostos pesquisados (não testados em humanos)

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  • 3,3-Difenilciclobutanamina (1978)[50]
  • 3,4-Diclorotametralina (trans-(1R,4S)-sertralina ) (1980)[51]
  • D-161 (2008)[52]
  • Desmetilsertralina - metabólito ativo da sertralina;afinidade 76 nM paraSERT, 420 nM paraNET, 440 nM paraDAT[53]
  • DMNPC (2000)[54]
  • DOV-102.677 (2006–2011)[13]
  • GSK1360707F (2010)[55][56]
  • Indatralina (1985)[57]
  • JNJ-7925476 (2008; apareceu pela primeira vez em 1987)[58]
  • JZ-IV-10 (2005)[59]
  • JZAD-IV-22 (2010)[60]
  • LR-5182 (1978)[61][62][63]
  • Metilnaftidato (HDMP-28) (2001)[64]
  • MI-4[65][66]
  • PRC200-SS (2008)[67]
  • SKF-83.959 (2013)[68]
  • TP1 (2011)[69]
  • Vários feniltropanos, como WF-23, dicloropano e RTI-55[70]
  • NS9775[71]

Extratos botânicos

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Referências

  1. ↑Millan, MJ (2009).«Dual- and triple-acting agents for treating core and co-morbid symptoms of major depression: Novel concepts, new drugs».Neurotherapeutics.6: 53–77.PMC 5084256Acessível livremente.PMID 19110199.doi:10.1016/j.nurt.2008.10.039 
  2. ↑Kulkarni, SK; Dhir, A (2009). «Current investigational drugs for major depression».Expert Opinion on Investigational Drugs.18: 767–88.PMID 19426122.doi:10.1517/13543780902880850 
  3. ↑Guiard, BP; El Mansari, M; Blier, P (2009). «Prospect of a dopamine contribution in the next generation of antidepressant drugs: The triple reuptake inhibitors».Current Drug Targets.10: 1069–84.PMID 19702555.doi:10.2174/138945009789735156 
  4. ↑Marks, DM; Pae, CU; Patkar, AA (2008).«Triple reuptake inhibitors: The next generation of antidepressants».Current Neuropharmacology.6: 338–43.PMC 2701280Acessível livremente.PMID 19587855.doi:10.2174/157015908787386078 
  5. ↑abChen, Z; Skolnick, P (2007). «Triple uptake inhibitors: Therapeutic potential in depression and beyond».Expert Opinion on Investigational Drugs.16: 1365–77.PMID 17714023.doi:10.1517/13543784.16.9.1365 
  6. ↑abMillan, MJ (2006). «Multi-target strategies for the improved treatment of depressive states: Conceptual foundations and neuronal substrates, drug discovery and therapeutic application».Pharmacology & Therapeutics.110: 135–370.PMID 16522330.doi:10.1016/j.pharmthera.2005.11.006 
  7. ↑Perona, MT; Waters, S; Hall, FS; Sora, I; Lesch, KP; Murphy, DL; Caron, M; Uhl, GR (2008).«Animal models of depression in dopamine, serotonin, and norepinephrine transporter knockout mice: Prominent effects of dopamine transporter deletions».Behavioural Pharmacology.19: 566–74.PMC 2644662Acessível livremente.PMID 18690111.doi:10.1097/FBP.0b013e32830cd80f 
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  39. ↑EP 0756596 
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  69. ↑Tian, JW; Jiang, WL; Zhong, Y; Meng, Q; Gai, Y; Zhu, HB; Hou, J; Xing, Y; Li, YX (2011). «Preclinical pharmacology of TP1, a novel potent triple reuptake inhibitor with antidepressant properties».Neuroscience.196: 124–30.PMID 21925241.doi:10.1016/j.neuroscience.2011.08.064 
  70. ↑Carroll, FI (2003). «2002 Medicinal Chemistry Division Award address: Monoamine transporters and opioid receptors. Targets for addiction therapy».Journal of Medicinal Chemistry.46: 1775–94.PMID 12723940.doi:10.1021/jm030092d 
  71. ↑Andreasen, Jesper T.; Redrobe, John P.; Nielsen, Elsebet Ø.; Christensen, Jeppe K.; Olsen, Gunnar M.; Peters, Dan (2013). «A combined α7 nicotinic acetylcholine receptor agonist and monoamine reuptake inhibitor, NS9775, represents a novel profile with potential benefits in emotional and cognitive disturbances».Neuropharmacology.73: 183–191.ISSN 0028-3908.PMID 23748055.doi:10.1016/j.neuropharm.2013.04.060 
  72. ↑Fehske, C. J.; Leuner, K.; Müller, W. E. (2009). «Ginkgo biloba extract (EGb761®) influences monoaminergic neurotransmission via inhibition of NE uptake, but not MAO activity after chronic treatment».Pharmacological Research.60: 68–73.PMID 19427589.doi:10.1016/j.phrs.2009.02.012 
  73. ↑Mechan, Annis O.; Fowler, Ann; Seifert, Nicole; Rieger, Henry; Wöhrle, Tina; Etheve, Stéphane; Wyss, Adrian; Schüler, Göde; Colletto, Biagio (2010). «Monoamine reuptake inhibition and mood-enhancing potential of a specified oregano extract».British Journal of Nutrition.105: 1150–1163.ISSN 0007-1145.PMID 21205415.doi:10.1017/S0007114510004940 
  74. ↑Sasaki, Kazunori; El Omri, Abdelfatteh; Kondo, Shinji; Han, Junkyu; Isoda, Hiroko (2013). «Rosmarinus officinalis polyphenols produce anti-depressant like effect through monoaminergic and cholinergic functions modulation».Behavioural Brain Research.238: 86–94.ISSN 0166-4328.PMID 23085339.doi:10.1016/j.bbr.2012.10.010 
  75. ↑Jin, Zeng-Liang; Gao, Nana; Zhou, Dan; Chi, Mu-Gen; Yang, Xue-Mei; Xu, Jiang-Ping (2012). «The extracts of Fructus Akebiae, a preparation containing 90% of the active ingredient hederagenin: Serotonin, norepinephrine and dopamine reuptake inhibitor».Pharmacology Biochemistry and Behavior.100: 431–439.ISSN 0091-3057.PMID 22005599.doi:10.1016/j.pbb.2011.10.001 
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