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Elzasonan









Elzasonan


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Elzasonan
Elzasonan structure.svg
Clinical data
Routes of
administration		 Oral
ATC code
  • none
Legal status
Legal status

  • In general: uncontrolled
Identifiers
CAS Number

  • 220322-05-4 ☑Y

PubChem CID

  • 19544192

  • 6914152
ChemSpider
  • 5290108
UNII
  • 933PJL964R
Chemical and physical data
Formula
C22H23Cl2N3OS
Molar mass 448.4085 g/mol
3D model (JSmol)
  • Interactive image

.mw-parser-output .nobold{font-weight:normal}
  (verify)

Elzasonan (CP-448,187) is a selective 5-HT1B and 5-HT1D receptor antagonist that was under development by Pfizer for the treatment of depression but was discontinued, possibly due to poor efficacy.[1][2][3][4][5] By preferentially blocking 5-HT1B and 5-HT1Dautoreceptors, elzasonan is thought to enhance serotonergic innervations originating from the raphe nucleus, thereby improving signaling to limbic regions like the hippocampus and prefrontal cortex and ultimately resulting in antidepressant effects.[3]



See also[edit]



  • GR-127,935

  • SB-649,915



References[edit]





  1. ^ José Miguel Vela; Helmut Buschmann; Jörg Holenz; Antonio Párraga; Antoni Torrens (2007). Antidepressants, Antipsychotics, Anxiolytics: From Chemistry and Pharmacology to Clinical Application. Weinheim: Wiley-VCH. ISBN 3-527-31058-4..mw-parser-output cite.citation{font-style:inherit}.mw-parser-output q{quotes:"""""""'""'"}.mw-parser-output code.cs1-code{color:inherit;background:inherit;border:inherit;padding:inherit}.mw-parser-output .cs1-lock-free a{background:url("//upload.wikimedia.org/wikipedia/commons/thumb/6/65/Lock-green.svg/9px-Lock-green.svg.png")no-repeat;background-position:right .1em center}.mw-parser-output .cs1-lock-limited a,.mw-parser-output .cs1-lock-registration a{background:url("//upload.wikimedia.org/wikipedia/commons/thumb/d/d6/Lock-gray-alt-2.svg/9px-Lock-gray-alt-2.svg.png")no-repeat;background-position:right .1em center}.mw-parser-output .cs1-lock-subscription a{background:url("//upload.wikimedia.org/wikipedia/commons/thumb/a/aa/Lock-red-alt-2.svg/9px-Lock-red-alt-2.svg.png")no-repeat;background-position:right .1em center}.mw-parser-output .cs1-subscription,.mw-parser-output .cs1-registration{color:#555}.mw-parser-output .cs1-subscription span,.mw-parser-output .cs1-registration span{border-bottom:1px dotted;cursor:help}.mw-parser-output .cs1-hidden-error{display:none;font-size:100%}.mw-parser-output .cs1-visible-error{font-size:100%}.mw-parser-output .cs1-subscription,.mw-parser-output .cs1-registration,.mw-parser-output .cs1-format{font-size:95%}.mw-parser-output .cs1-kern-left,.mw-parser-output .cs1-kern-wl-left{padding-left:0.2em}.mw-parser-output .cs1-kern-right,.mw-parser-output .cs1-kern-wl-right{padding-right:0.2em}


  2. ^ Stahl's essential psychopharmacology: neuroscientific basis and practical applications. Cambridge, UK: Cambridge University Press. 2008. ISBN 0-521-85702-3.


  3. ^ ab "IngentaConnect 5-HT1 Receptor Augmentation Strategies as Enhanced Efficacy Thera..."


  4. ^ "Pfizer, Inc.: analysis of patenting 1998 – 2001; Expert Opinion on Therapeutic Patents - 12(5):Pages 725-732 - Informa Healthcare".


  5. ^ "Discontinued psychiatric drugs in 2008; Expert Opinion on Investigational Drugs - 18(10):Pages 1431-1443 - Informa Healthcare".














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