Alsactide

From Wikipedia the free encyclopedia

Alsactide
Clinical data
ATC code
Identifiers
CAS Number
PubChem CID
ChemSpider
UNII
KEGG
CompTox Dashboard (EPA)
ECHA InfoCard100.047.442 Edit this at Wikidata
Chemical and physical data
FormulaC99H155N29O21S
Molar mass2119.57 g·mol−1
3D model (JSmol)
  • [H]/N=C(\N)/NCCC[C@@H](C(=O)N[C@@H](Cc1c[nH]c2c1cccc2)C(=O)NCC(=O)N[C@@H](CCCCN)C(=O)N3CCC[C@H]3C(=O)N[C@@H](C(C)C)C(=O)NCC(=O)N[C@@H](CCCCN)C(=O)N[C@@H](CCCCN)C(=O)N[C@@H](CCCCN)C(=O)NCCCCN)NC(=O)[C@H](Cc4ccccc4)NC(=O)[C@H](Cc5cnc[nH]5)NC(=O)[C@H](CCC(=O)O)NC(=O)[C@H](CCSC)NC(=O)[C@H](CO)NC(=O)[C@H](Cc6ccc(cc6)O)NC(=O)CCN
  • InChI=1S/C99H155N29O21S/c1-59(2)84(97(148)113-56-81(132)115-68(26-10-14-40-101)87(138)119-69(27-11-15-41-102)88(139)118-67(25-9-13-39-100)85(136)109-45-18-17-43-104)127-96(147)79-30-20-47-128(79)98(149)73(28-12-16-42-103)116-82(133)55-112-86(137)76(51-62-53-111-66-24-8-7-23-65(62)66)124-89(140)70(29-19-46-110-99(106)107)120-93(144)75(49-60-21-5-4-6-22-60)123-94(145)77(52-63-54-108-58-114-63)125-90(141)71(35-36-83(134)135)121-91(142)72(38-48-150-3)122-95(146)78(57-129)126-92(143)74(117-80(131)37-44-105)50-61-31-33-64(130)34-32-61/h4-8,21-24,31-34,53-54,58-59,67-79,84,111,129-130H,9-20,25-30,35-52,55-57,100-105H2,1-3H3,(H,108,114)(H,109,136)(H,112,137)(H,113,148)(H,115,132)(H,116,133)(H,117,131)(H,118,139)(H,119,138)(H,120,144)(H,121,142)(H,122,146)(H,123,145)(H,124,140)(H,125,141)(H,126,143)(H,127,147)(H,134,135)(H4,106,107,110)/t67-,68-,69-,70-,71-,72-,73-,74-,75-,76-,77-,78-,79-,84-/m0/s1
  • Key:DIDCGVRALANKIU-OTEFFYEFSA-N
  (verify)

Alsactide (INN) (brand name Synchrodyn 1-17 or simply Synchrodyn, former development code name Hoechst 433), also known as alisactide, is a synthetic peptide and analogue of adrenocorticotropic hormone (ACTH) which is used in Italy as a diagnostic agent in kidney function for adrenal insufficiency.[1][2][3] Like ACTH, alsactide is thought to act as a non-selective agonist of the melanocortin receptors, including the ACTH receptor (MC2R).[1][citation needed] However, it appears to show a different profile of receptor selectivity relative to ACTH, as it apparently demonstrated no evidence of inhibition of endogenous ACTH in Addison's disease patients.[4]

See also[edit]

References[edit]

  1. ^ Elks J (14 November 2014). The Dictionary of Drugs: Chemical Data: Chemical Data, Structures and Bibliographies. Springer. pp. 34–. ISBN 978-1-4757-2085-3.
  2. ^ Index Nominum 2000: International Drug Directory. Taylor & Francis. January 2000. pp. 33–. ISBN 978-3-88763-075-1.
  3. ^ Morton IK, Hall JM (6 December 2012). Concise Dictionary of Pharmacological Agents: Properties and Synonyms. Springer Science & Business Media. pp. 12–. ISBN 978-94-011-4439-1.
  4. ^ Kontogeorgos G (1 January 2004). Molecular Pathology of the Pituitary. Karger Medical and Scientific Publishers. pp. 66–. ISBN 978-3-8055-7740-3.