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Meet Our California Scientists F. Javier Piedrafita
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F. Javier Piedrafita

F. Javier PiedrafitaTorreyPinesInstituteCA

Associate Member
Cancer Cell Biology

858.597.3884 - phone
858.597.3804 - fax
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The Nuclear Hormone Receptor (NHR) superfamily of transcription factors mediate signaling by a diverse array of vitamins, hormones, and small molecules to regulate the expression of specific target genes involved in many important biological functions, such as development, metabolism, homeostasis, cell growth and differentiation, and others.  NHRs regulate gene expression in coordination with an increasing number of coregulators (corepressors and coactivators).  Many NHRs are involved in a variety of human diseases, including cancer.  Thus ligands of RAR/RXRs (retinoids), steroid receptors (ER, AR), PPARs and others have been pursued as novel targeted therapies for the chemoprevention and treatment of cancers, including prostate, breast, lung, colon cancers as well as hematologic malignancies.  Dr. Piedrafita has been working for the last decade on the mechanism of action of a family of synthetic retinoids called retinoid-related molecules (RRMs) or adamantly arotinoids (AdArs) that show strong anticancer activity.  This lead to the discovery that certain AdArs induced tumor cell apoptosis independently of RAR/RXR activity, but rather by inhibiting protein kinases that are often hyperactivated in cancer, such as IKK-2.  Given the RAR-mediated toxicity of classical retinoids, research is now focused in optimizing lead AdArs to eliminate RAR activity while enhancing IKK-2 inhibitory activity.  Most recently, Dr. Piedrafita’s interest has been expanded to the identification and characterization of novel ligands of orphan receptors and other NHRs with strong connection in cancer.


1985: Universidad Autónoma de Madrid, Spain, B.S. in Biology.
1992: Universidad Autónoma de Madrid, Spain, Ph.D. in Biochemistry and Molecular Biology.

Academic Postions:

  • February 2009-present: Torrey Pines Institute for Molecular Studies, San Diego, CA. Associate Member.
  • April 2008 - present: Gerinda Therapeutics, Inc., San Diego, CA. Director of Biology Research.
  • 1999 - 2003: Maxia Pharmaceuticals, Inc., San Diego, CA. Consultant.
  • April 1998 - present: Sidney Kimmel Cancer Center, San Diego, CA. Assistant Professor.
  • 1996 - 1998: Sidney Kimmel Cancer Center, San Diego, CA. Assistant Member, Adjunct.
  • 1994 - 1995: Sidney Kimmel Cancer Center, San Diego, CA. Postdoctoral associate.
  • 1992 - 1994: La Jolla Cancer Research Foundation, La Jolla, CA. Postdoctoral fellow.
  • 1989, April-July. Trinity College, Dublin (Ireland). Visiting student.
  • 1986 - 1991: Instituto de Química Orgánica, CSIC, Madrid (Spain). PhD student.
  • 1984 - 1986: Centro de Biología Molecular, CSIC-UAM, Madrid (Spain). Graduate student.

Professional Affiliations

Honors and Awards

  • 1994-95: Postdoctoral fellowship (MEC).
  • 1993: CAJA MADRID Award for the Doctoral Thesis.
  • 1989: Short term fellowship for short stays at foreign countries (MEC).
  • 1988-91: Predoctoral fellowship (MEC).
  • 1987: ANTIBIOTICOS, S.A. Award, by the Spanish Society of Therapeutic Chemistry

Selected Publications (10 of 28)

  1. S. Pérez-Rodríguez, M.A. Ortiz, J. García, R. Pereira, F. Rodríguez-Barrios, A.R. de Lera, and F.J. Piedrafita.  Highly Twisted Adamantyl Arotinoids. Synthesis, antiproliferative effects and RXR transactivation profiles.  Eur. J. Med. Chem. (2009), 44: 2434-2446.
  2. P. Lorenzo, R. Alvarez, M.A. Ortiz, S. Alvarez, F.J. Piedrafita, and A.R. de Lera.  Inhibition of IkappaB kinase-β and anticancer activities of novel chalcone adamantyl arotinoids.  J. Med. Chem. (2008), 51: 5431-5440.
  3. F.J. Piedrafita, and M.A. Ortiz.  Mechanism of action and therapeutic potential of novel adamantyl retinoid-related molecules.  Current Cancer Therapy Reviews, (2006), 2:185-198.
  4. Y. Bayon, M.A. Ortiz, F.J. Lopez-Hernandez, P.H. Howe, and F.J. Piedrafita. The retinoid antagonist MX781 induces clusterin expression in prostate cancer cells via heat shock factor-1 and activator protein-1 transcription factors.  Cancer Research, (2004), 64:5905-5912.
  5. A. Kumar, F.J. Piedrafita, and W.F. Reynolds.  PPARγ ligands regulate MPO expression by an estrogen-dependent mechanism involving the -463 G/A promoter polymorphism.  Journal of Biological Chemistry, (2004), 279:8300-8315.
  6. F.J. Lopez-Hernandez, M.A. Ortiz, Y. Bayon, and F.J. Piedrafita. Retinoid-related molecules require caspase 9 for the effective release of Smac and the rapid induction of apoptosis.  Cell Death and Differentiation, (2004), 11:154-164.
  7. Y. Bayon, M.A. Ortiz, F.J. Lopez-Hernandez, F. Gao, M. Karin, M. Pfahl, and F.J. Piedrafita. Inhibition of IΚB kinase by a new class of retinoid-related anticancer agents that induce apoptosis.  Molecular and Cellular Biology, (2003), 23: 1061-1074.
  8. M.A. Ortiz, F.J. Lopez-Hernandez, Y. Bayon, M. Pfahl, and F.J. Piedrafita. Retinoid-related Molecules Induce Cytochrome c Release and Apoptosis through Activation of c-Jun NH(2)-Terminal Kinase/p38 Mitogen-activated Protein Kinases.  Cancer Research, (2001), 61: 8504-8512.
  9. M.A. Ortiz, F.J. Piedrafita, M. Pfahl and R. Maki. TOR: A new orphan receptor expressed in the thymus that can modulate retinoid and thyroid hormone signals. Molecular Endocrinology, (1995), 9: 1679-1691.
  10. F.J. Piedrafita, I. Bendik, M.A. Ortiz & M. Pfahl. Thyroid hormone receptor homodimers can function as ligand-sensitive repressors. Molecular Endocrinology, (1995), 9: 563-578.