Clinical Focus

  • Internal Medicine

Academic Appointments

Administrative Appointments

  • Assistant Professor of Medicine, Stanford University (1985 - 1993)
  • White House Fellow, Washington, DC (1993 - 1994)
  • Senior Consultant, The Advisory Board, Washington DC (1994 - 1995)
  • Director of Medical Affairs, Heartport - Redwood City, CA (1995 - 1999)
  • Healthcare Consultant, . (1999 - 2004)
  • Senior Director, Clinical Research, KAI Pharmaceuticals, Inc (2004 - 2007)
  • Co-Director, SPARK Program (2008 - Present)

Professional Education

  • Board Certification: Internal Medicine, American Board of Internal Medicine (1985)
  • Residency:Stanford University School of Medicine (1985) CA
  • Internship:Stanford University School of Medicine (1983) CA
  • Medical Education:Brown University Program (1982) RI
  • MA, Santa Clara University, Pastoral Ministries (2007)
  • MD, Brown University, School of Medicine (1982)
  • MBA, Stanford University-GSB, Health Management (1993)
  • BS, Brown University, Biological Sciences (1979)

All Publications

  • Protein kinase C, an elusive therapeutic target? NATURE REVIEWS DRUG DISCOVERY Mochly-Rosen, D., Das, K., Grimes, K. V. 2012; 11 (12): 937-957


    Protein kinase C (PKC) has been a tantalizing target for drug discovery ever since it was first identified as the receptor for the tumour promoter phorbol ester in 1982. Although initial therapeutic efforts focused on cancer, additional indications--including diabetic complications, heart failure, myocardial infarction, pain and bipolar disorder--were targeted as researchers developed a better understanding of the roles of eight conventional and novel PKC isozymes in health and disease. Unfortunately, both academic and pharmaceutical efforts have yet to result in the approval of a single new drug that specifically targets PKC. Why does PKC remain an elusive drug target? This Review provides a short account of some of the efforts, challenges and opportunities in developing PKC modulators to address unmet clinical needs.

    View details for DOI 10.1038/nrd3871

    View details for Web of Science ID 000311895800021

    View details for PubMedID 23197040

  • Myocardial salvage in acute myocardial infarction - Challenges in clinical translation JOURNAL OF MOLECULAR AND CELLULAR CARDIOLOGY Mochly-Rosen, D., Grimes, K. V. 2011; 51 (4): 451-453

    View details for DOI 10.1016/j.yjmcc.2011.08.002

    View details for Web of Science ID 000295302900006

    View details for PubMedID 21851825

  • Intracoronary KAI-9803 as an adjunct to primary percutaneous coronary intervention for acute ST-segment elevation myocardial infarction CIRCULATION Roe, M. T., Hartmann, F., LINS, J., Batchelor, W., Ruzyllo, W., Kochman, J., Armstrong, B., Buszman, P., Buszman, P., Leisch, F., Baran, K., Roubin, G., Zenni, M., Bilodeau, L., Caputo, R., Chu, A., Lombardi, W., Adamus, J., Hermiller, J., Darius, H., Krzeminska-Pakula, M., Saucedo, J., Simek, S., Zmudka, K., Farah, T., Hauptmann, K., Lee, D., Lemos, P., Rohrbeck, S., Moshage, W., Strasser, R., Albirini, A., Anderson, E., Bode, C., Caramori, P., Eaton, G., Hoffman, S., Huber, K., Khoury, S., Miller, J., Peterson, J., Porizka, V., Rivera, E., Roe, M., Schuster, P., Stasek, J., Zago, A. 2008; 117 (7): 886-896


    KAI-9803, a delta-protein kinase C inhibitor, has been shown to ameliorate injury associated with ischemia and reperfusion in animal models of acute myocardial infarction (MI).Direct Inhibition of delta-Protein Kinase C Enzyme to Limit Total Infarct Size in Acute Myocardial Infarction (DELTA MI) was a "first-in-human," dose-escalation study that evaluated the safety, tolerability, and activity of KAI-9803 for patients with acute anterior ST-segment elevation MI undergoing primary percutaneous coronary intervention. Patients who presented within 6 hours of symptom onset and had an occluded left anterior descending infarct artery on angiography were randomized in a 2:1 fashion to receive 1 of 4 doses of KAI-9803 (cohort 1, 0.05 mg; cohort 2, 0.5 mg; cohort 3, 1.25 mg; cohort 4, 5.0 mg) versus blinded concurrent placebo delivered in 2 divided doses via intracoronary injection before and after reestablishment of antegrade epicardial flow with percutaneous coronary intervention. Safety and biomarker end points were assessed. Overall, 154 patients were randomized and treated with study drug (37 in cohort 1, 38 in cohort 2, 38 in cohort 3, 41 in cohort 4). The incidence of serious adverse events was similar between patients treated with KAI-9803 versus placebo. Other safety end points, including changes in QT intervals and standard laboratory values after study drug administration, were similar between treatment groups. Although the study was not powered to demonstrate efficacy with the biomarker end points assessed, signs of drug activity with KAI-9803 were suggested by trends for consistent, nonsignificant reductions in creatine kinase-MB area under the curve and ST-recovery area under the curve values across all dosing cohorts with KAI-9803 compared with concurrent placebo, and similar trends were demonstrated for improvements in (99m)technetium sestamibi infarct size values with active study drug in cohorts 1, 2, and 3.KAI-9803 had an acceptable safety and tolerability profile when delivered via intracoronary injection during primary percutaneous coronary intervention for ST-segment elevation MI. Signs of potential drug activity were demonstrated with biomarker end points in this small exploratory study, indicating that further testing of KAI-9803 as an adjunctive therapy for ST-segment elevation MI is warranted.

    View details for DOI 10.1161/CIRCULATIONAHA.107.759167

    View details for Web of Science ID 000253428100005

    View details for PubMedID 18250271

  • Recognition, diagnosis, and treatment of primary focal hyperhidrosis JOURNAL OF THE AMERICAN ACADEMY OF DERMATOLOGY Hornberger, J., Grimes, K., NAUMANN, M., Glaser, D. A., Lowe, N. J., Naver, H., Ahn, S., Stolman, L. R. 2004; 51 (2): 274-286

    View details for DOI 10.1016/j.jaad.2003.12.029

    View details for Web of Science ID 000223005600014

    View details for PubMedID 15280848



    Hematopoietic growth factors have been used to accelerate engraftment after bone marrow transplantation and to "mobilize" peripheral blood progenitor cells (PBPC). We report on the data in 85 consecutive patients with Hodgkin's disease who were treated in a single institution using different methods to obtain PB progenitor cells. Use of granulocyte colony-stimulating factor for mobilization resulted in a significantly accelerated time to recovery of granulocytes (10 days v 12 days, P < .01) when compared with "nonmobilized" PBPC recipients. Similarly, use of mobilized PBPC resulted in a significantly accelerated time to platelet engraftment (13 days v 30 days, P < .001) when compared with "nonmobilized" recipients. Moreover, there was a statistically significant difference in total costs in favor of the group receiving "mobilized" PBPC.

    View details for Web of Science ID A1993KY00500008

    View details for PubMedID 7682454