EMA401

EMA401
Clinical data
Routes of
administration		Oral
Legal status
Legal status
  • Phase II Clinical Trials
Pharmacokinetic data
Bioavailability33%
Protein bindingAngiotensin II Subtype 2 Receptor
Elimination half-life6-12 hr
Identifiers
  • (S)-2-(Diphenylacetyl)-1,2,3,4-tetrahydro-6-methoxy-5-(phenylmethoxy)-3-isoquinolinecarboxylic acid
CAS Number
PubChem CID
ChemSpider
UNII
ChEBI
ChEMBL
CompTox Dashboard (EPA)
Chemical and physical data
FormulaC32H29NO5
Molar mass507.586 g·mol−1
3D model (JSmol)
Specific rotation+
Density1.256±0.06 g/cm3
Boiling point745.3 ± 60.0 °C (1,373.5 ± 108.0 °F)
Solubility in water14 mg/mL (20 °C)
  • COC1=C(C2=C(CN(C(C2)C(=O)O)C(=O)C(C3=CC=CC=C3)C4=CC=CC=C4)C=C1)OCC5=CC=CC=C5
  • InChI=1S/C32H29NO5/c1-37-28-18-17-25-20-33(31(34)29(23-13-7-3-8-14-23)24-15-9-4-10-16-24)27(32(35)36)19-26(25)30(28)38-21-22-11-5-2-6-12-22/h2-18,27,29H,19-21H2,1H3,(H,35,36)
  • Key:GHBCIXGRCZIPNQ-UHFFFAOYSA-N

EMA401 is a drug under development for the treatment of peripheral neuropathic pain. Trials were discontinued in 2015, with new trials scheduled to begin March, 2018.[1] It was initially established as a potential drug option for patients suffering pain caused by postherpetic neuralgia.[2] It may also be useful for treating various types of chronic neuropathic pain [3] EMA401 has shown efficacy in preclinical models of shingles, diabetes, osteoarthritis, HIV and chemotherapy.[4][5][6][7] EMA401 is a competitive antagonist of angiotensin II type 2 receptor (AT2R) being developed by the Australian biotechnology company Spinifex Pharmaceuticals. EMA401 target angiotensin II type 2 receptors, which may have importance for painful sensitisation.[8]

  1. ^ "EMA401 clinical trials". clinicaltrials.gov. Retrieved 2017-02-10.
  2. ^ Rice AS, Dworkin RH, McCarthy TD, Anand P, Bountra C, McCloud PI, et al. (May 2014). "EMA401, an orally administered highly selective angiotensin II type 2 receptor antagonist, as a novel treatment for postherpetic neuralgia: a randomised, double-blind, placebo-controlled phase 2 clinical trial". Lancet. 383 (9929): 1637–1647. doi:10.1016/S0140-6736(13)62337-5. PMID 24507377. S2CID 9396522.
  3. ^ Sumners C, Horiuchi M, Widdop RE, McCarthy C, Unger T, Steckelings UM (August 2013). "Protective arms of the renin-angiotensin-system in neurological disease". Clinical and Experimental Pharmacology & Physiology. 40 (8): 580–588. doi:10.1111/1440-1681.12137. PMID 23735163. S2CID 11323149.
  4. ^ WO patent 2006066361, Smith MT, Wyse BD, "Methods of Treatment or Prophylaxis", published 2006-06-29 
  5. ^ WO patent 2011088504, MCCARTHY THOMAS DAVID; BAKER ANDREW RAINSFORD, "METHODS AND COMPOSITIONS FOR IMPROVED NERVE CONDUCTION VELOCITY", published 2006-06-29 
  6. ^ Sumners C, Horiuchi M, Widdop RE, McCarthy C, Unger T, Steckelings UM (August 2013). "Protective arms of the renin-angiotensin-system in neurological disease". Clinical and Experimental Pharmacology & Physiology. 40 (8): 580–588. doi:10.1111/1440-1681.12137. PMID 23735163. S2CID 11323149.
  7. ^ Anand U, Facer P, Yiangou Y, Sinisi M, Fox M, McCarthy T, et al. (August 2013). "Angiotensin II type 2 receptor (AT2 R) localization and antagonist-mediated inhibition of capsaicin responses and neurite outgrowth in human and rat sensory neurons". European Journal of Pain. 17 (7): 1012–1026. doi:10.1002/j.1532-2149.2012.00269.x. PMC 3748799. PMID 23255326.
  8. ^ WO patent 2006066361, Smith MT, Wyse BD, "Methods of Treatment or Prophylaxis", published 2006-06-29