Cytokinetics Presents Research Data from Heart Failure Program

Additional Presentations at the American Society of Cell Biology Meeting Span Multiple Therapeutic Areas

South San Francisco, CA - December 8, 2004

Cytokinetics, Inc. (Nasdaq: CYTK) announced today that four of the eleven poster presentations that the company made this week at the 44th Annual American Society of Cell Biology (ASCB) Meeting in Washington, DC relate to its congestive heart failure program. The heart failure program presentations provide further preclinical support for the novel mechanism of directly stimulating the activity of the cardiac myosin motor protein as a potential next-generation approach to managing acute and chronic congestive heart failure. In addition, the findings support the hypothesis that drug candidates arising from this research program may address certain mechanistic liabilities of existing pharmaceuticals by increasing cardiac contractility without increasing intracellular calcium or inhibiting phosphodiesterase activity, each of which may be associated with adverse clinical effects. Cytokinetics is currently planning to move a compound from this program into Phase I human clinical trials for congestive heart failure in 2005.

The presentations related to the company's congestive heart failure program were as follows:

· "Activation of Cardiac Sarcomere ATPase by CK-1122534, a Small Molecule Agent that Specifically Targets Cardiac Myosin" was presented on Sunday, December 5, 2004. This presentation covered experiments that characterized the mechanism of action of CK-1122534, a small molecule activator of cardiac myosin discovered at Cytokinetics, in a series of steady-state and transient kinetic biochemical assays. This presentation concluded that this experimental compound can activate the ATPase of cardiac myosin in various reconstituted systems and in skinned cardiac myofibrils, that this activation is specific for cardiac myosin and that it involves an acceleration of actin-dependent phosphate release.

· "The Cardiac Myosin Activator, CK-1122534, Overcomes the Myosin II Inhibitors 2, 3-Butanedione-2-Monoxime and (-)-S-Blebbistatin without Affecting the Ca2+ Transient in Ventricular Myocytes," was presented on Tuesday, December 7, 2004. This presentation summarized work in cardiac myocytes designed to further characterize the mechanism of action of CK-1122534 indicating that the cardiac myosin activator can overcome the inhibition of ventricular myocyte contractility by the myosin inhibitors, blebbistatin and 2, 3-Butanedione-2-Monoxime (BDM).

· "The Cardiac Myosin Activator, CK-1122534, Increases Contractility in Adult Cardiac Myocytes without Altering the Calcium Transient," was presented on Tuesday, December 7, 2004. This presentation concluded that CK-1122534 increases the fractional shortening in ventricular myocytes (a measure of cardiac contractility) in a dose-dependent manner, does not increase the calcium transient, does not inhibit phosphodiesterase (PDE) activity and is active in the presence of a beta-adrenergic blocker.

· "Cellular Responses of the Myosin Activator CK-0689705 in Normal and Heart Failure Models," was presented on Tuesday, December 7, 2004. This presentation concluded that the cardiac myosin activator, CK-0689705, increases the fractional shortening in ventricular myocytes in a dose-dependent manner, does not increase the calcium transient and increases contractility in ventricular myocytes from rats with defined heart failure.

"We are pleased to have the opportunity to present these research findings," stated David Morgans, Jr., Ph.D., Cytokinetics; Senior Vice President of Drug Discovery and Development. "Building on the data we recently presented at the 2004 Scientific Sessions of the American Heart Association (AHA) in November, these presentations add to the breadth and depth of the mechanistic profile of cardiac myosin activators, spanning elegant enzymological characterization through studies using myocytes from an animal model of heart failure. We are pleased with the progress of this program in optimizing and advancing multiple lead candidates and look forward to moving a drug candidate into human clinical trials in 2005."

Other Presentations

Cytokinetics also announced the presentation of seven additional poster presentations at the ASCB conference. Cumulatively, these presentations are indicative of the company's progress derived from fruitful research across multiple classes of protein families in the cytoskeleton that further elucidates the identity, roles and regulation of potential cytoskeletal targets involved in actin dynamics and microtubule dynamics in the pathogenic yeast, Candida albicans, the malarial parasite, Plasmodium falciparum, and mammalian cells. These presentations covered a broad variety of areas that could provide valuable insight to advance research and drug discovery across multiple therapeutic areas including cancer, cardiovascular diseases, fungal infections and malaria.

“These poster presentations are the result of our focus on research in the cytoskeleton,” stated James Sabry, M.D., Ph.D., President and Chief Executive Officer at Cytokinetics. “When we started the company over six years ago, we knew that the cytoskeleton would provide a rich area for potential next-generation pharmaceuticals. We are very excited about the maturation of the company programs having leveraged this expertise in cytoskeletal biology and pharmacology into clinical programs in oncology and cardiovascular disease and a strong research pipeline.”

Background on the Cytoskeleton

The cytoskeleton is a diverse, multicomponent framework upon which the cell interior is ordered. As such it plays a fundamental role in all aspects of cell mechanics including cell division, intracellular transport, cell motility and the establishment and regulation of cell polarity and organization. In many ways, this framework can be considered to be analogous to a highly organized city plan, where cellular activities are regulated in systematized locations connected by highways upon which components are transported by motor cars. However, in the case of cells, the cytoskeletal highways are protein structures called microtubules and microfilaments and the motor cars are enzymes, termed molecular motors, which more recently have been discovered to generate the mechanical forces critical to cellular function. The cytoskeleton has been implicated in a variety of disease pathologies, ranging from cancer to cardiovascular diseases to infectious diseases.

About Cytokinetics

Cytokinetics is a leading biopharmaceutical company focused on the discovery, development and commercialization of novel small molecule drugs that specifically target the cytoskeleton. The cytoskeleton is a complex biological infrastructure that plays a fundamental role within every human cell. Cytokinetics' focus on the cytoskeleton enables it to develop novel and potentially safer and more effective classes of drugs directed at treatments for cancer, cardiovascular disease, fungal diseases and other diseases. Cytokinetics has developed a cell biology driven approach and proprietary technologies to evaluate the function of many interacting proteins in the complex environment of the intact human cell. Cytokinetics employs the PUMA™ system and Cytometrix™ technologies to enable early identification and automated prioritization of compounds that are highly selective for their intended protein targets without other cellular effects, and are thereby less likely to give rise to clinical side effects. Cytokinetics and GlaxoSmithKline have entered into a strategic alliance to discover, develop and commercialize small molecule therapeutics targeting human mitotic kinesins for applications in the treatment of cancer and other diseases. GlaxoSmithKline is conducting Phase II and Phase Ib clinical trials for SB-715992 and a Phase I clinical trial for SB-743921, each a drug candidate that has emerged from the strategic alliance. Additional information about Cytokinetics can be obtained at www.cytokinetics.com.

This press release contains forward-looking statements for purposes of the Private Securities Litigation Reform Act of 1995 (the "Act"). Cytokinetics disclaims any intent or obligation to update these forward-looking statements, and claims the protection of the Safe Harbor for forward-looking statements contained in the Act. Examples of such statements include, but are not limited to, statements relating to the expected timing, scope and results of our clinical development and research programs and statements regarding the potential benefits of our drug candidates and potential drug candidates and the enabling capabilities of our proprietary technologies. Such statements are based on management's current expectations, but actual results may differ materially due to various factors. Such statements involve risks and uncertainties, including, but not limited to, those risks and uncertainties relating to difficulties or delays in development, testing, regulatory approval, production and marketing of Cytokinetics' drug candidates that could slow or prevent clinical development, product approval or market acceptance (including the risks related to uncertainty of patent protection for Cytokinetics' intellectual property or trade secrets, Cytokinetics' ability to obtain additional financing if necessary and unanticipated research and development and other costs). For further information regarding these and other risks related to Cytokinetics' business, investors should consult Cytokinetics' filings with the Securities and Exchange Commission.