Miproxifene

In this article we will explore the phenomenon of Miproxifene and its impact on contemporary society. Since its appearance, Miproxifene has sparked debates, conflicting opinions and has generated deep interest in different areas. Over the years, Miproxifene has evolved and taken on new dimensions, influencing not only the way we interact with the world around us, but also our perception of reality. Through detailed analysis, we will address the various facets of Miproxifene and examine its relevance in the current context.
Miproxifene
Clinical data
Other namesDP-TAT-59
Identifiers
  • 4-phenyl]-2-(4-propan-2-ylphenyl)but-1-enyl]phenol
CAS Number
PubChem CID
ChemSpider
UNII
ChEMBL
CompTox Dashboard (EPA)
Chemical and physical data
FormulaC29H35NO2
Molar mass429.604 g·mol−1
3D model (JSmol)
  • CC/C(=C(\C1=CC=C(C=C1)O)/C2=CC=C(C=C2)OCCN(C)C)/C3=CC=C(C=C3)C(C)C
  • InChI=1S/C29H35NO2/c1-6-28(23-9-7-22(8-10-23)21(2)3)29(24-11-15-26(31)16-12-24)25-13-17-27(18-14-25)32-20-19-30(4)5/h7-18,21,31H,6,19-20H2,1-5H3/b29-28-
  • Key:FVVPWVFWOOMXEZ-ZIADKAODSA-N

Miproxifene (INN) (former developmental code name DP-TAT-59) is a nonsteroidal selective estrogen receptor modulator (SERM) of the triphenylethylene group that was never marketed.[1][2] It is a derivative of afimoxifene (4-hydroxytamoxifen) in which an additional 4-isopropyl group is present in the β-phenyl ring.[3] The drug has been found to be 3- to 10-fold more potent than tamoxifen in inhibiting breast cancer cell growth in in vitro models.[1][4][5] Miproxifene is the active metabolite of miproxifene phosphate (TAT-59), a phosphate ester and prodrug of miproxifene that was developed to improve its water solubility.[1][2][6][7] Miproxifene phosphate was under development for the treatment of breast cancer and reached phase III clinical trials for this indication but development was discontinued.[1]

References

  1. ^ a b c d "Miproxifene". AdisInsight. Springer Nature Switzerland AG.
  2. ^ a b Stella V, Borchardt R, Hageman M, Oliyai R, Maag H, Tilley J (12 March 2007). Prodrugs: Challenges and Rewards. Springer Science & Business Media. pp. 168–169. ISBN 978-0-387-49782-2.
  3. ^ Oettel M, Schillinger E (6 December 2012). Estrogens and Antiestrogens I: Physiology and Mechanisms of Action of Estrogens and Antiestrogens. Springer Science & Business Media. pp. 58–60. ISBN 978-3-642-58616-3.
  4. ^ Kelloff GJ, Hawk ET, Sigman CC (17 August 2008). Cancer Chemoprevention: Volume 2: Strategies for Cancer Chemoprevention. Springer. pp. 251–. ISBN 978-1-59259-768-0.
  5. ^ Ottow E, Weinmann H (8 September 2008). Nuclear Receptors as Drug Targets. John Wiley & Sons. pp. 90–. ISBN 978-3-527-62330-3.
  6. ^ Stromgaard K, Krogsgaard-Larsen P, Madsen U (19 August 2016). Textbook of Drug Design and Discovery, Fifth Edition. CRC Press. pp. 162–. ISBN 978-1-4987-0279-9.
  7. ^ Yang HC, Yeh WK, McCarthy JR (22 November 2013). Enzyme Technologies: Pluripotent Players in Discovering Therapeutic Agent. Wiley. pp. 166–. ISBN 978-1-118-73989-1.


Stub icon

This drug article relating to the genito-urinary system is a stub. You can help Wikipedia by expanding it.

Stub icon

This antineoplastic or immunomodulatory drug article is a stub. You can help Wikipedia by expanding it.

Wikious
Boobota
Sagapedia