Oral Presentation at the 2008 Scientific Sessions of the American HeartAssociation

The oral presentation entitled, "The Selective Cardiac Myosin Activator,CK-1827452, Increases Systolic Function in a Concentration-Dependent Mannerin Patients with Stable Heart Failure" was presented in a CardiovascularSeminar (#117) entitled "Translational Trials and Strategies: First in Man"on Sunday, November 9, 2008, by John Cleland, MD, FACC, FRCP, FESC,Professor of Cardiology, Castle Hill Hospital, University of Hull, UnitedKingdom. The presentation included data from 28 patients (eight patientsfrom each of Cohorts 1, 2 and 3 and four patients from Cohort 4) in thisongoing clinical trial.

These interim analyses demonstrated statistically significant increases insystolic ejection time (p < 0.0001) and fractional shortening (p < 0.05) atCK-1827452 plasma concentrations greater than 100 ng/mL, and statisticallysignificant increases in stroke volume (p < 0.01) at CK-1827452 plasmaconcentrations greater than 200 ng/mL. In addition, there werestatistically significant correlations between increasing CK-1827452 plasmaconcentration and increases in systolic ejection time, stroke volume,fractional shortening (all p < 0.0001), and cardiac output (p < 0.01).There were also statistically significant correlations between increasingCK-1827452 concentration and decreases in supine and standing heart rate(both p < 0.0001) and left ventricular end-systolic volume (p < 0.05).

Ejection fraction was calculated by two different methods. The firstrelies exclusively on two-dimensional (2D) echocardiographic imaging tomeasure left ventricular end-systolic and end-diastolic volumes. In thesecond, "hybrid" method, stroke volume (measured using Doppler technology)is divided by the left ventricular end-diastolic volume (assessed by 2Dechocardiography). There were statistically significant correlationsbetween increasing CK-1827452 plasma concentration and increases inejection fraction by both methods (p < 0.05 for the 2D method; p < 0.0001for the hybrid method); furthermore, increases in ejection fraction by thehybrid method achieved statistical significance at CK-1827452 plasmaconcentrations greater than 300 ng/mL.

"I am pleased to have the opportunity to present these data at theScientific Sessions of the American Heart Association. In particular,additional analysis of the ejection fraction using Doppler-derived strokevolume now demonstrates that this cardiac myosin activator appears toimprove all major indices of cardiac systolic function in stable heartfailure patients," stated Dr. Cleland. "This novel drug candidate offers apotentially exciting new advance in the treatment of heart failure, whichis a debilitating disease affecting millions of people worldwide."

"We continue to be encouraged by the progress of the clinical trialsprogram and by the growing body of human clinical data for CK-1827452,"stated Andrew A. Wolff, MD, FACC, Cytokinetics' Senior Vice President ofClinical Research and Development and Chief Medical Officer. "CK-1827452offers a potential therapeutic option for patients suffering from heartfailure, a disease with high mortality and morbidity that costs the healthcare system billions of dollars in re-hospitalizations and lostproductivity."

Development Status of CK-1827452

CK-1827452 is currently the subject of a clinical trials program comprisedof multiple Phase I and Phase IIa trials. This program is designed toevaluate the safety, tolerability, pharmacodynamics and pharmacokineticprofile of both intravenous and oral formulations of CK-1827452 for thepotential treatment of heart failure across the continuum of care, in bothhospital and outpatient settings. CK-1827452 is the subject of three PhaseIIa clinical trials. The first clinical trial is the above-referencedongoing Phase IIa clinical trial of CK-1827452 in patients with stableheart failure. The second clinical trial is a Phase IIa trial that isdesigned to evaluate an intravenous formulation together with an oralformulation of CK-1827452 in patients with ischemic cardiomyopathy andangina. The third clinical trial is an open-label Phase IIa clinical trialthat is designed to evaluate an intravenous formulation of CK-1827452 inpatients with stable heart failure undergoing clinically indicated coronaryangiography in the cardiac catheterization laboratory

In addition, Cytokinetics has conducted five Phase I clinical trials ofCK-1827452 in healthy subjects: a first-time-in-humans study evaluating anintravenous formulation, an oral bioavailability study evaluating bothintravenous and oral formulations, and three studies of oral formulations:a drug-drug interaction study, a dose proportionality study and a studyevaluating modified-release formulations. Data from each of these trialshave been reported previously.

Background on Cardiac Myosin Activators and Cardiac Contractility

Cardiac myosin is the cytoskeletal motor protein in the cardiac muscle cellthat is directly responsible for converting chemical energy into themechanical force resulting in cardiac contraction. Cardiac contractilityis driven by the cardiac sarcomere, a highly ordered cytoskeletal structurecomposed of cardiac myosin, actin and a set of regulatory proteins, and isthe fundamental unit of muscle contraction in the heart. The sarcomererepresents one of the most thoroughly characterized protein machines inhuman biology. Cytokinetics' cardiovascular program is focused towards thediscovery and development of small molecule cardiac myosin activators inorder to create next-generation treatments to manage acute and chronicheart failure. Cytokinetics' program is based on the hypothesis thatactivators of cardiac myosin may address certain mechanistic liabilities ofexisting positive inotropic agents by increasing cardiac contractilitywithout increasing intracellular calcium. Current inotropic agents, suchas beta-adrenergic receptor agonists or inhibitors of phosphodiesteraseactivity, increase cardiac cell contractility by increasing theconcentration of intracellular calcium, which further activates the cardiacsarcomere. This effect on calcium levels, however, also has been linked topotentially life-threatening side effects. The inotropic mechanism ofcurrent drugs also increases the velocity of cardiac contraction andshortens systolic ejection time. In contrast, cardiac myosin activatorshave been shown to work in the absence of changes in intracellular calciumby a novel mechanism that directly stimulates the activity of the cardiacmyosin motor protein. Cardiac myosin activators accelerate therate-limiting step of the myosin enzymatic cycle and shift the enzymaticcycle in favor of the force-producing state. This inotropic mechanismresults not in an increase in the velocity of cardiac contraction, butinstead, in a lengthening of the systolic ejection time, which results inincreased cardiac contractility and cardiac output in a potentially moreoxygen-efficient manner.

Background on the Heart Failure Market

Heart failure is a debilitating syndrome affecting millions of people inthe United States. The growing prevalence of heart failure translates intohigh hospitalization rates and associated societal costs. In 2004, over5 million patients carried a diagnosis of chronic heart failure in theUnited States alone. Many of these patients with chronic heart failuresuffer episodic deterioration. The number of diagnosed events of acuteheart failure was over 4 million in 2004. These numbers are increasing dueto the aging population and an increased likelihood of survival after acutemyocardial infarction. The costs to society and the individual attributableto the prevalence of heart failure are high. The annual direct and indirectcosts of heart failure on the nation's health care system are estimated tobe $35 billion in 2008. A portion of that cost comes from heart failuredrugs used to treat both chronic and acute heart failure. Sales of drugs totreat heart failure reached over $1.6 billion in 2004, including$1.3 billion for chronic heart failure and $0.3 billion for acute heartfailure. Despite currently available therapies, readmission rates forpatients remain as high as 42% within one year of hospital discharge andmortality rates are approximately 60% over the five-year period following adiagnosis of chronic heart failure. The limited effectiveness of currenttherapies points to the need for next-generation therapeutics that mayoffer improved efficacy without increased adverse events.

About Cytokinetics

Cytokinetics is a biopharmaceutical company focused on the discovery,development and commercialization of novel small molecule drugs that mayaddress areas of significant unmet clinical needs. Cytokinetics'cardiovascular disease program is focused to cardiac myosin, a motorprotein essential to cardiac muscle contraction. Cytokinetics' leadcompound from this program, CK-1827452, a novel small molecule cardiacmyosin activator, entered Phase II clinical trials for the treatment ofheart failure in 2007. Under a strategic alliance established in 2006,Cytokinetics and Amgen Inc. are performing joint research focused onidentifying and characterizing activators of cardiac myosin as back-up andfollow-on potential drug candidates toCK-1827452. Amgen has obtained an option for an exclusive license todevelop and commercialize CK-1827452, subject to Cytokinetics' developmentand commercial participation rights. Cytokinetics' cancer program isfocused on mitotic kinesins, a family of motor proteins essential to celldivision. Under a strategic alliance established in 2001, Cytokinetics andGlaxoSmithKline (GSK) are conducting research and development activitiesfocused on the potential treatment of cancer. Cytokinetics is developingtwo novel drug candidates that have arisen from this program, ispinesib andSB-743921, each a novel inhibitor of kinesin spindle protein (KSP), amitotic kinesin. Cytokinetics is conducting the Phase I portion of a PhaseI/II clinical trial of ispinesib as monotherapy as a first-line treatmentin chemotherapy-naïve patients with locally advanced or metastatic breastcancer. In addition, Cytokinetics is conducting the Phase I portion of aPhase I/II trial ofSB-743921 in patients with non-Hodgkin or Hodgkin lymphoma. GSK has anoption for the joint development and commercialization of ispinesib andSB-743921. GSK-923295, an inhibitor of centromere-associated protein E(CENP-E) inhibitor, is being developed under the strategic alliance by GSK;GSK began a Phase I clinical trial with GSK-923295 in 2007. In April 2008,Cytokinetics announced the selection of a potential drug candidate directedtowards skeletal muscle contractility which may be developed as a potentialtreatment for skeletal muscle weakness associated with neuromusculardiseases or other conditions. All of these drug candidates and potentialdrug candidates have arisen from Cytokinetics' research activities and aredirected towards the cytoskeleton. The cytoskeleton is a complex biologicalinfrastructure that plays a fundamental role within every human cell.Additional information about Cytokinetics can be obtained atwww.cytokinetics.com.

This press release contains forward-looking statements for purposes of thePrivate Securities Litigation Reform Act of 1995 (the "Act"). Cytokineticsdisclaims any intent or obligation to update these forward-lookingstatements, and claims the protection of the Act's safe harbor forforward-looking statements. Examples of such statements include, but arenot limited to, statements relating to Cytokinetics' research anddevelopment programs, including the design, conduct and results of itsclinical trials for CK-1827452 and the potential significance of suchresults; the size and growth of potential markets for drug candidatesarising out of Cytokinetics' heart failure program, including forCK-1827452; and the properties and potential clinical benefits of CK-1827452 and Cytokinetics' other drug candidates and potential drugcandidates, including CK-1827452's potential effects on cardiac systolicfunction. Such statements are based on management's current expectations,but actual results may differ materially due to various risks anduncertainties, including, but not limited to, potential difficulties ordelays in the development, testing, regulatory approval or production ofCK-1827452 or Cytokinetics' other drug candidates that could slow orprevent clinical development or product approval, including risks thatcurrent and past results of clinical trials or preclinical studies may notbe indicative of future clinical trials results, patient enrollment for orconduct of clinical trials may be difficult or delayed, including, but notlimited to, difficulties or delays due to political instability incountries where clinical trials ofCK-1827452 or Cytokinetics' other drug candidates are being conducted,CK-1827452 or Cytokinetics' other drug candidates may have adverse sideeffects or inadequate therapeutic efficacy, the U.S. Food and DrugAdministration or foreign regulatory agencies may delay or limitCytokinetics' or its partners' ability to conduct clinical trials, andCytokinetics may be unable to obtain or maintain patent or trade secretprotection for its intellectual property; Cytokinetics may incurunanticipated research and development and other costs or be unable toobtain additional financing necessary to conduct development of itsproducts; standards of care may change and others may introduce products oralternative therapies for the treatment of indications CK-1827452 orCytokinetics' other drug candidates and potential drug candidates maytarget; and risks and uncertainties relating to Amgen's and GSK's decisionsas to whether to exercise their respective options and the timing andreceipt of payments, including option fees, milestones and royalties onfuture potential product sales under Cytokinetics' respective agreementswith Amgen and GSK. For further information regarding these and other risksrelated to Cytokinetics' business, investors should consult Cytokinetics'filings with the Securities and Exchange Commission.

Contact:Christopher S. KeenanDirector, Investor Relations(650) 624-3000