Merck to present multiple clinical studies of dinaciclib at ASH Annual Meeting

Ligand Pharmaceuticals Incorporated (NASDAQ:LGND) today announced that multiple clinical studies of dinaciclib (SCH 727965) will be presented by Merck at the upcoming 52nd American Society of Hematology (ASH) Annual Meeting being held in Orlando, Florida at the Orange County Convention Center, December 4-7, 2010.

“Dinaciclib (SCH727965) Is a Novel Cyclin Dependent Kinase Inhibitor That Promotes Selective Apoptosis In CLL Cells and Abrogates the Protective Effects of Microenvironment Cytokines”

Dinaciclib is a pro-apoptotic inhibitor of cyclin-dependent kinases being evaluated by Merck for the potential treatment of cancer. In connection with Ligand's acquisition of Pharmacopeia, dinaciclib is derived from a collaboration initiated in 1998 between Pharmacopeia and Schering-Plough Ltd.

Poster Presentation on December 4, 2010, 5:30 PM-7:30 PM in Hall A3/A4:

• "Update on the Phase I Study of the Cyclin Dependent Kinase Inhibitor Dinaciclib (SCH 727965) In Patients with Relapsed or Refractory Chronic Lymphocytic Leukemia (CLL): Confirmation of Clinical Activity and Feasibility of Long-Term Administration" (Abstract # 1396, Poster board #: I-376)

Poster Presentations on December 6, 2010 in Hall A3/A4:

6:00 p.m. - 8:00 p.m.

• Phase II Study of the Cyclin-Dependent Kinase (CDK) Inhibitor Dinaciclib (SCH 727965) In Patients with Advanced Acute Leukemias" (Abstract # 3287, Poster board #: III-66)
• "Early Evidence of Anti-Lymphoma Activity of the Cyclin Dependent Kinase Inhibitor Dinaciclib (SCH 727965) In Heavily Pre-Treated Low Grade Lymphoma and Diffuse Large Cell Lymphoma Patients" (Abstract # 3966, Poster board #: III-745)
• "Single Agent Activity of the Cyclin-Dependent Kinase (CDK) Inhibitor Dinaciclib (SCH 727965) In Acute Myeloid and Lymphoid Leukemia Cells" (Abstract # 3981, Poster board #: III-760)

Oral Session on December 7, 2010 in 304 ABCD:

• 8:30 a.m. - "Dinaciclib (SCH727965) Is a Novel Cyclin Dependent Kinase Inhibitor That Promotes Selective Apoptosis In CLL Cells and Abrogates the Protective Effects of Microenvironment Cytokines" (Abstract # 971)