Praveen Rajendran

Praveen Rajendran

Assistant Professor

Center for Epigenetics & Disease Prevention
2121 W. Holcombe Blvd.
Houston, TX   77030-3303

Phone: 713-677-7803
Fax: 713-677-7784

Education and Training

Praveen Rajendran received his Bachelor of Pharmacy (B. Pharm) degree with Honors in 1994 and his Ph.D. degree in Pharmacology in 2006 from Birla Institute of Technology & Science (BITS), Pilani, India. He earned a Post Graduate Diploma in Business Management (MBA equivalent) in 1998 from IMT-G, India. After completing doctoral studies Dr. Rajendran spent three years in Pharma R&D from 2006-09, where he was part of preclinical development teams in Cancer biology. He carried out his post-doctoral work at the Linus Pauling Institute, Oregon State University from 2009-13. Dr. Rajendran joined the faculty as an Assistant Professor in 2014 in the Center for Epigenetics and Disease Prevention (CEDP), Institute of Biosciences and Technology, Texas A&M University Health Science Center, Houston, Texas.

Research Interests

In addition to genetic changes, epigenetic mechanisms play an important role in tumor development. Among the different epigenetic mechanisms, modulators of histone deacetylase (HDAC) activity have shown promise in the clinic, both as cancer chemopreventive and therapeutic agents. Studies conducted by Dr. Rajendran and colleagues have identified turnover of HDACs as a novel mechanism by which dietary isothiocyanates (ITCs) inhibited the growth of colon cancer cells. Recent work has shown how dietary ITCs that can affect the epigenome can also lead to protein acetylation, for example DNA repair proteins, and modify DNA damage and repair responses, specifically in cancer cells but not normal cells.

Current research, including appropriate clinical investigation, will clarify these emerging concepts and reveal the potential of dietary agents for chemo and/or radio sensitization in cancer. Future work will involve proteomic analyses of the cellular acetylome to identify novel targets that result from deacetylase (DAC) inhibition, discovery of novel HDAC inhibitors through structure activity relationship studies and pharmacokinetic-pharmacodynamic (PK/PD) correlations between metabolites generated in target organ and putative HDAC inhibition. These findings would be corroborated in clinically-relevant models for GI cancers, including diseases that have unmet needs. Overall, these studies have the potential to contribute to the new field of Nutri-epigenomics and to better understand the importance of epigenetic mechanisms in cancer prevention and treatment.

Selected Publications

Rajendran P, Dashwood WM, Li L, Kang Y, Kim E, Johnson G, Fischer KA, Löhr CV, Williams DE, Ho E, Yamamoto M, Lieberman DA, Dashwood RH. Nrf2 status affects tumor growth, HDAC3 gene promoter associations, and the response to sulforaphane in the colon. Clin Epigenetics. 2015 Sep 18;7(1):102.

Kim E, Bisson WH, Löhr CV, Williams DE, Ho E, Dashwood RH, Rajendran P. Histone and Non-Histone Targets of Dietary Deacetylase Inhibitors. Curr Top Med Chem. 2016; 16(7):714-31.

Balasubramanian G, Kilambi N, Rathinasamy S, Rajendran P, Narayanan S, Rajagopal S. Quinolone-based HDAC inhibitors. J Enzyme Inhib Med Chem. 2014 Aug;29(4):555-62.

Rajendran P, Kidane A, Yu TW, Dashwood M, Williams DE, Ho E, Dashwood RH. HDAC turnover, CtIP acetylation, and dysregulated DNA damage signaling in colon cancer cells treated with sulforaphane and related dietary isothiocyanates. Epigenetics. 2013 Jun;8(6):612-23.

Rajendran P, Ho E, Williams DE, Dashwood RH. Dietary phytochemicals, HDAC inhibition, and DNA damage/repair defects in cancer cells. Clinical Epigenetics 2011, 3:4.

Rajendran P, Delage B, Dashwood WM, Yu TW, Wuth B, Williams DE, Ho E,  Dashwood RH. Histone deacetylase turnover and recovery in sulforaphane-treated colon cancer cells: competing actions of 14-3-3 and Pin1 in HDAC3/SMRT corepressor complex dissociation/reassembly. Mol. Cancer, 2011, May 30;10(1):68.

Rajendran P, Williams DE, Ho E, Dashwood RH. Metabolism as a key to histone deacetylase inhibition. Crit. Rev. Biochem. Mol. Biol. 2011; 46(3):181-99.

Rajendran P, Jaggi M, Singh MK, Mukherjee R, Burman AC. Pharmacological evaluation of C-3 modified Betulinic acid derivatives with potent anticancer activity. Invest New Drugs. 2008 Feb;26(1):25-34.

Jaggi M, Prasad S, Singh AT, Praveen R, Dutt S, Mathur A, Sharma R, Gupta N, Ahuja R, Mukherjee R, Burman AC. Anticancer activity of a peptide combination in gastrointestinal cancers targeting multiple neuropeptide receptors. Invest New Drugs. 2008 Dec;26(6):489-504.

Mukherjee R, Jaggi M, Rajendran P, Siddiqui MJ, Srivastava SK, Vardhan A, Burman AC. Betulinic acid and its derivatives as anti-angiogenic agents. Bioorg Med Chem Lett. 2004 May 3;14(9):2181-4.

For a complete list of publications, please visit:

US Patents

  1. Histone deacetylase inhibitors. 8,476,255. July 2, 2013.
  2. Histone deacetylase inhibitors. 8,450,525. May 28, 2013.
  3. Biocompatible, non-biodegradable, non-toxic polymer useful for nanoparticle pharmaceutical compositions. 8,338,562. December 25, 2012.
  4. Betulinic acid derivatives. 8,022,055. September 20, 2011.
  5. Antiangiogenic drugs. 6,492,330. December 10, 2002.
  6. Betulinic acid derivatives having antiangiogenic activity, processes for producing such derivatives and their use for treating tumor associated angiogenesis 6,403,816. June 11, 2002.
  7. Antiangiogenic activity of betulinic acid and its derivatives. 6,228,850. May 8, 2001.