"We are pleased that these data could be shared with the scientific community at the AACR-NCI-EORTC International Conference on Molecular Targets and Cancer Therapeutics," stated David J. Morgans, PhD, Cytokinetics' Executive Vice President of Preclinical Research and Development. "These results underscore the potential for GSK-923295 in combination with other innovative cancer drug candidates. We look forward to further exploring the potential for this novel drug candidate with GlaxoSmithKline as we together evaluate data from this ongoing clinical trial."

Presentations at the AACR-NCI-EORTC International Conference on Molecular Targets and Cancer Therapeutics

A poster titled "Synergistic Interaction Between CENP-E inhibitor GSK923295 and MEK inhibitor GSK1120212" was presented by Yan Y. Degenhardt, Ph.D., GlaxoSmithKline on Tuesday, November 17, 2009. This poster presentation summarized a non-clinical study evaluating the combination of the CENP-E inhibitor, GSK-923295, and a MEK inhibitor, GSK-1120212, to determine if this combination might improve clinical efficacy over either compound as a single agent in selected tumors. This study identified multiple genes along the MAPK pathway as hits in a synthetic lethal siRNA library screen for GSK-923295, suggesting that inhibiting the MAPK pathway may enhance sensitivity of cells to GSK-923295. The combination of these two drug candidates was tested by fixed-ratio dosing in 5 colon cell lines, 15 lung cell lines and 8 pancreas lines. Synergy between these two drug candidates was observed in most of the cell lines using one or more judging criteria; there was no association with genetic background (RAS/PIK3CA). Finally, as measured by caspase assay, more apoptosis was induced in the presence of both drugs than either alone.

A poster and oral presentation titled "RNAi-directed Identification of Chemosensitizers of GSK923295 Response" was presented by Holly Yin, Ph.D., Associate Investigator, Pharmaceutical Genomics Division of The Translational Genomics Research Institute, Phoenix, AZ on Wednesday, November 18. The poster and oral presentation summarized a non-clinical study designed to identify chemosensitizers for GSK-923295. The authors concluded that RNAi phenotype profiling of non-small cell lung cancer cells identified significant pathways that suggest synergistic opportunities with GSK-923295. Combination synergy was observed with small molecule MAPK inhibitors targeting genes that were validated from the HT-RNAi screen. New gene targets were identified that are sensitizing candidates for GSK-923295 and that provide a rationale for continued investigation in future clinical studies. This study suggests that both siRNA knockdown and drug synergy can be successfully applied towards the development of clinical therapeutics.

Development Status of GSK-923295 and Background on CENP-E

GSK-923295 is a small-molecule inhibitor of centromere-associated protein E (CENP-E), and the third novel drug candidate to arise from Cytokinetics' broad strategic alliance with GlaxoSmithKline (GSK). In August 2007, GSK initiated a first-time-in-humans, Phase I clinical trial of GSK-923295. This trial is an open-label, non-randomized, dose-finding trial designed to investigate the safety, tolerability, pharmacodynamics and pharmacokinetic profile of GSK-923295 in patients with advanced, refractory solid tumors.

CENP-E plays an essential role in chromosome movement during early mitosis and integrates mitotic spindle mechanics with regulators of the mitotic checkpoint; hence CENP-E is directly involved in coupling the mechanics of mitosis with the mitotic checkpoint signaling machinery, regulating cell-cycle transition from metaphase to anaphase. CENP-E is also essential for prometaphase chromosome movements that contribute to metaphase chromosome alignment. These processes are essential to cell proliferation. CENP-E is expressed exclusively in proliferating cells and is abundant during mitosis; it is absent from non-proliferating cells, including neurons. Inhibition of CENP-E induces cell cycle arrest in mitosis with bipolar mitotic spindles and misaligned chromosomes leading to subsequent apoptosis. GSK-923295 is the first drug candidate to enter human clinical trials that specifically targets CENP-E.

About Cytokinetics

Cytokinetics is a clinical-stage biopharmaceutical company focused on the discovery and development of small molecule therapeutics that modulate muscle function for the potential treatment of serious diseases and medical conditions. Cytokinetics' lead drug candidate from its cardiac muscle contractility program, omecamtiv mecarbil (formerly CK-1827452), is in Phase II clinical development for the potential treatment of heart failure. Amgen Inc. holds an exclusive license worldwide (excluding Japan) to develop and commercialize omecamtiv mecarbil and related compounds, subject to Cytokinetics' specified development and commercialization participation rights. Cytokinetics is independently developing CK-2017357, a skeletal muscle activator, as a potential treatment for diseases and conditions associated with aging, muscle wasting or neuromuscular dysfunction. CK-2017357 is in Phase I clinical development. Cytokinetics is also conducting non-clinical development of compounds that inhibit smooth muscle contractility and which may be useful as potential treatments for diseases and conditions such as systemic hypertension, pulmonary arterial hypertension or bronchoconstriction. In addition, prior Cytokinetics' research generated three anti-cancer drug candidates in Phase I clinical development: ispinesib, SB-743921 and GSK-923295. Cytokinetics is seeking a partner for ispinesib and SB-743921. GSK-923295 is being developed by GlaxoSmithKline in collaboration with Cytokinetics. All of these drug candidates and potential drug candidates have arisen from Cytokinetics' research activities and are directed towards the cytoskeleton. The cytoskeleton is a complex biological infrastructure that plays a fundamental role within every human cell. 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 initiation, scope, design, conduct and results of Cytokinetics' and its partners' research and development programs, including the significance of results of non-clinical studies relating to GSK-923295, and the potential benefits of GSK-923295 and Cytokinetics' other drug candidates and potential drug candidates. Such statements are based on management's current expectations, but actual results may differ materially due to various risks and uncertainties, including, but not limited to, potential difficulties or delays in the development, testing, regulatory approvals for trial commencement, progression or product sale or manufacturing, or production of Cytokinetics' drug candidates that could slow or prevent clinical development or product approval, including risks that current and past results of clinical trials or preclinical studies may not be indicative of future clinical trials results, patient enrollment for or conduct of clinical trials may be difficult or delayed, Cytokinetics' drug candidates may have adverse side effects or inadequate therapeutic efficacy, the U.S. Food and Drug Administration or foreign regulatory agencies may delay or limit Cytokinetics' or its partners' ability to conduct clinical trials, and Cytokinetics may be unable to obtain or maintain patent or trade secret protection for its intellectual property; Cytokinetics may incur unanticipated research and development and other costs or be unable to obtain additional financing necessary to conduct development of its products; Cytokinetics may be unable to enter into future collaboration agreements for its drug candidates and programs on acceptable terms, if at all; standards of care may change, rendering Cytokinetics' drug candidates obsolete; others may introduce products or alternative therapies for the treatment of indications Cytokinetics' drug candidates and potential drug candidates may target; and risks and uncertainties relating to the timing and receipt of payments from its partners, including milestones and royalties on future potential product sales under Cytokinetics' collaboration agreements with such partners. For further information regarding these and other risks related to Cytokinetics' business, investors should consult Cytokinetics' filings with the Securities and Exchange Commission.

Contacts:

Cytokinetics, Incorporated
Christopher S. Keenan (Investors and Media)
Director, Investor Relations
(650) 624-3000

SOURCE: Cytokinetics, Inc.

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Oral Presentations

An oral presentation titled "Inhibition of Smooth Muscle Myosin, a Novel Anti-Hypertensive Strategy" was presented on Monday, November 16, 2009 by Fady Malik, MD, PhD, FACC, Vice President, Biology and Therapeutics, Cytokinetics, Inc., South San Francisco, California. This presentation summarized non-clinical research evaluating smooth muscle myosin inhibitors in models of hypertension. The authors concluded that smooth muscle myosin inhibition reduced vascular resistance and lowered blood pressure in a canine model of hypertension. In addition, the pattern of regional vasodilation is different for a specific smooth muscle myosin inhibitor, CK-2018448, as compared to the calcium channel blocker, amlodipine. For CK-2018448, blood flow to the kidney increased without change in blood flow to the limb. In contrast, for amlodipine, the largest increases in blood flow were found in the limb. The authors concluded that the smooth muscle myosin inhibitor and the calcium channel blocker elicited different patterns of regional vasodilation. In addition, the renal vasodilation induced by smooth muscle myosin inhibition could have salutary effects in conditions accompanied by renal insufficiency such as hypertension, acute heart failure, and acute renal failure due to an interruption of adequate blood flow to the kidney.

An oral presentation titled "A Direct Inhibitor of Smooth Muscle Myosin as a Novel Therapeutic Approach for the Treatment of Pulmonary Artery Hypertension" was presented on Tuesday, November 17, 2009 by Malarvannan Pannirselvam, M.V.Sc., Ph.D., Scientist, Cytokinetics, Inc., South San Francisco, California. This presentation summarized a non-clinical study designed to test the hypothesis that direct inhibition of smooth muscle myosin should provide a novel and effective means of relaxing vascular smooth muscle. In this study, the authors concluded that CK-2018571, a smooth muscle myosin inhibitor, selectively inhibited the ATPase activity of smooth muscle myosin and relaxed contracted arteriovascular tissue rings as a consequence of direct inhibition of smooth muscle myosin. In addition, CK-2018571 relaxed pulmonary arterial rings from MCT-PAH rats suggesting its potential use as a vasodilator in pulmonary arterial hypertension. Finally, an active pro-drug of CK-2018571, CK-2019165, decreased the elevated right ventricular systolic pressure in two animal models of pulmonary arterial hypertension. The authors concluded that these data together support the hypothesis that direct inhibition of smooth muscle myosin could be a novel therapeutic approach for the treatment of pulmonary arterial hypertension.

Poster Presentation

A poster presentation titled "Inhibition of Smooth Muscle Myosin, a Novel Therapeutic Approach for Pulmonary Hypertension" was presented on Tuesday, November 17, 2009 by David Ho, MD, CV Dynamics and the Department of Cell Biology and Molecular Medicine and Cardiovascular Research Institute, New Jersey Medical School, University of Medicine and Dentistry of New Jersey, Newark, NJ from 9:30 AM - 11:00 AM Eastern Time. This poster summarized a non-clinical study designed to establish a porcine model of acute pulmonary arterial hypertension, by either hypoxia or administration of a thromboxane analog, and to examine the extent to which the inhibition of smooth muscle myosin by CK-2019165 administered either intravenously or by inhalation is able to ameliorate pulmonary hypertension in chronically instrumented pigs. The authors concluded that CK-2019165, delivered intravenously at a dose of 4 mg/kg, reduced (p < 0.01) the increased pulmonary vascular resistance in both hypoxia and thromboxane models, respectively. Mean arterial pressure fell modestly and heart rate rose slightly in the conscious state. In addition, in the hypoxia model, CK-2019165 was delivered via inhalation and the increased pulmonary vascular resistance fell similarly while mean arterial pressure and heart rate were unchanged. The maximum extent of vasodilation was similar to that produced with sodium nitroprusside. The authors concluded that inhibition of smooth muscle myosin may be a novel therapeutic approach to the treatment of pulmonary arterial hypertension.

Background on Cytokinetics Smooth Muscle Contractility Program

In January 2009, Cytokinetics announced the selection of a small molecule inhibitor of smooth muscle myosin for development. Cytokinetics' smooth muscle research program is directed to smooth muscle myosin, the motor protein responsible for the contraction of the smooth muscle cells that surround airways in the lungs and the blood vessels that control blood pressure. By inhibiting the function of the myosin motor central to the contraction of smooth muscle, these potent small molecules directly lead to the relaxation of contracted smooth muscle. Cytokinetics' smooth myosin inhibitors have demonstrated encouraging pharmacological activity in preclinical models that may relate to uses for the potential treatment of diseases such as systemic hypertension, pulmonary arterial hypertension, asthma and chronic obstructive pulmonary disease (COPD). Cytokinetics continues to progress smooth muscle myosin inhibitors in non-clinical development activities.

About Cytokinetics

Cytokinetics is a clinical-stage biopharmaceutical company focused on the discovery and development of small molecule therapeutics that modulate muscle function for the potential treatment of serious diseases and medical conditions. Cytokinetics' lead drug candidate from its cardiac muscle contractility program, omecamtiv mecarbil (formerly CK-1827452), is in Phase II clinical development for the potential treatment of heart failure. Amgen Inc. holds an exclusive license worldwide (excluding Japan) to develop and commercialize omecamtiv mecarbil and related compounds, subject to Cytokinetics' specified development and commercialization participation rights. Cytokinetics is independently developing CK-2017357, a skeletal muscle activator, as a potential treatment for diseases and conditions associated with aging, muscle wasting or neuromuscular dysfunction. CK-2017357 is in Phase I clinical development. Cytokinetics is also conducting non-clinical development of compounds that inhibit smooth muscle contractility and which may be useful as potential treatments for diseases and conditions such as systemic hypertension, pulmonary arterial hypertension or bronchoconstriction. In addition, prior Cytokinetics' research generated three anti-cancer drug candidates in Phase I clinical development: ispinesib, SB-743921 and GSK-923295. Cytokinetics is seeking a partner for ispinesib and SB-743921 and GSK-923295 is being developed under Cytokinetics' collaboration with GlaxoSmithKline. All of these drug candidates and potential drug candidates have arisen from Cytokinetics' research activities and are directed towards the cytoskeleton. The cytoskeleton is a complex biological infrastructure that plays a fundamental role within every human cell. 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 initiation, scope, design, conduct and results of Cytokinetics' research and development programs, including the significance of results of non-clinical studies relating to Cytokinetics' smooth muscle myosin inhibitors, and the potential benefits of Cytokinetics' drug candidates and potential drug candidates, including the potential utility of its smooth muscle myosin inhibitors for the treatment of pulmonary arterial hypertension, systemic hypertension and other diseases. Such statements are based on management's current expectations, but actual results may differ materially due to various risks and uncertainties, including, but not limited to, potential difficulties or delays in the development, testing, regulatory approvals for trial commencement, progression or product sale or manufacturing, or production of Cytokinetics' drug candidates that could slow or prevent clinical development or product approval, including risks that current and past results of clinical trials or preclinical studies may not be indicative of future clinical trials results, patient enrollment for or conduct of clinical trials may be difficult or delayed, Cytokinetics' drug candidates may have adverse side effects or inadequate therapeutic efficacy, the U.S. Food and Drug Administration or foreign regulatory agencies may delay or limit Cytokinetics' or its partners' ability to conduct clinical trials, and Cytokinetics may be unable to obtain or maintain patent or trade secret protection for its intellectual property; Cytokinetics may incur unanticipated research and development and other costs or be unable to obtain additional financing necessary to conduct development of its products; Cytokinetics may be unable to enter into future collaboration agreements for its drug candidates and programs on acceptable terms, if at all; standards of care may change, rendering Cytokinetics' drug candidates obsolete; others may introduce products or alternative therapies for the treatment of indications Cytokinetics' drug candidates and potential drug candidates may target; and risks and uncertainties relating to the timing and receipt of payments from its partners, including milestones and royalties on future potential product sales under Cytokinetics' collaboration agreements with such partners. For further information regarding these and other risks related to Cytokinetics' business, investors should consult Cytokinetics' filings with the Securities and Exchange Commission.

Contacts:

Cytokinetics, Incorporated
Christopher S. Keenan (Investors and Media)
Director, Investor Relations
(650) 624-3000

SOURCE: Cytokinetics, Inc.

Poster Presentations at AACR-NCI-EORTC Symposium:

Poster #B173: "Synergistic Interaction Between CENP-E inhibitor GSK923295 and MEKi Inhibitor GSK1120212," is scheduled to be displayed on Tuesday, November 17 from 12:30 PM - 2:30 PM Eastern Time in Halls C-D at the Poster Session B: New Molecular Targets 1. The poster will be presented by the author, Yan Y. Degenhardt, Ph.D., Manager, Cancer Metabolism, Oncology R&D,GlaxoSmithKline.

Poster #PR-10 "RNAi-directed Identification of Chemosensitizers of GSK923295 Response," is scheduled to be displayed on Wednesday, November 18 from 12:30 PM - 2:30 PM Eastern Time in Poster Session C: Pharmacogenetics, Pharmacogenomics, and Therapeutic Response in Halls C-D. The poster will be presented by the author, Holly Yin, Ph.D., Head of Cellular Genomics, Translational Genomics Research Institute (TGen).

Oral Presentation at AACR-NCI-EORTC Symposium:

"RNAi-directed Identification of Chemosensitizers of GSK923295 Response," is scheduled to be presented as part of the Proffered Paper Session on Wednesday, November 18 from 4:30 - 5:30 PM Eastern Time. The presentation will be made by Holly Yin, Ph.D., Head of Cellular Genomics, Translational Genomics Research Institute (TGen).

About Cytokinetics

Cytokinetics is a clinical-stage biopharmaceutical company focused on the discovery and development of small molecule therapeutics that modulate muscle function for the potential treatment of serious diseases and medical conditions. Cytokinetics' lead drug candidate from its cardiac muscle contractility program, omecamtiv mecarbil (formerly CK-1827452), is in Phase II clinical development for the potential treatment of heart failure. Amgen Inc. holds an exclusive license worldwide (excluding Japan) to develop and commercialize omecamtiv mecarbil and related compounds, subject to Cytokinetics' specified development and commercialization participation rights. Cytokinetics is independently developing CK-2017357, a skeletal muscle activator, as a potential treatment for diseases and conditions associated with aging, muscle wasting or neuromuscular dysfunction. CK-2017357 is in Phase I clinical development. Cytokinetics is also conducting non-clinical development of compounds that inhibit smooth muscle contractility and which may be useful as potential treatments for diseases and conditions such as systemic hypertension, pulmonary arterial hypertension or bronchoconstriction. In addition, prior Cytokinetics' research generated three anti-cancer drug candidates in Phase I clinical development: ispinesib, SB-743921 and GSK-923295. Cytokinetics is seeking a partner for ispinesib and SB-743921 and GSK-923295 is being developed under Cytokinetics' collaboration with GlaxoSmithKline. All of these drug candidates and potential drug candidates have arisen from Cytokinetics' research activities and are directed towards the cytoskeleton. The cytoskeleton is a complex biological infrastructure that plays a fundamental role within every human cell. 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 Act's safe harbor for forward-looking statements. Examples of such statements include, but are not limited to, statements relating to planned presentations and the properties and potential benefits of Cytokinetics' drug candidates and potential drug candidates. Such statements are based on management's current expectations, but actual results may differ materially due to various risks and uncertainties, including, but not limited to, potential difficulties or delays in the development, testing, regulatory approval and production of Cytokinetics' drug candidates and potential drug candidates that could slow or prevent clinical development or product approval, including risks that current and past results of clinical trials or preclinical studies may not be indicative of future clinical trials results and that Cytokinetics' drug candidates and potential drug candidates may have unexpected adverse side effects or inadequate therapeutic efficacy. For further information regarding these and other risks related to Cytokinetics' business, investors should consult Cytokinetics' filings with the Securities and Exchange Commission.

Contact:
Cytokinetics, Incorporated
Christopher S. Keenan (Investors and Media)
Director, Investor Relations
(650) 624-3000

SOURCE: Cytokinetics, Inc.