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Biotech / Medical : Biotech Valuation -- Ignore unavailable to you. Want to Upgrade?

To: former_pgs who wrote (14474)	12/4/2004 5:25:52 AM
From: JustTradeEm	Read Replies (1) \| Respond to of 52153

Thanks, I have no problem admitting I have little understanding of the science behind any biotech company. Had looked at CYTK based primarily on the fact that it appears to be building a base here under 9. The last time it broke out to the upside, a trade would have brought 30 - 40 %. Was wondering if next week's presentations could serve as a catalyst for CYTK. Appreciate your taking time to reply, thanks again. JTE

To: former_pgs who wrote (14474)	7/27/2005 12:02:48 PM
From: keokalani'nui	Read Replies (1) \| Respond to of 52153

former_pgs, cytk is out today with its poster on the MOA of its cardiac myosin program. If I correctly understood your post a while back ("Attempts to strengthen muscle contraction in the failing heart by increasing the sarcomeric ATPase (b-adrenergic receptor agonists) do not help survival."), it looks like it avoids history's mistakes: From cytk's PR: The poster titled, "Direct Activation of Cardiac Myosin, A Novel Mechanism for Improving Cardiac Function" (Poster Abstract Presentation #P136) was presented on Tuesday, July 26, 2005 at 5:00 pm Mountain Time. This presentation covered experiments that characterized the mechanism of action of CK-1213296, a small molecule activator of cardiac myosin discovered by Cytokinetics. The objective of this research was to discover and optimize molecules that improve cardiac function in a manner consistent with the therapeutic hypothesis, specifically that improving cardiac contractility by directly activating cardiac myosin can potentially address the liabilities of current inotropic drugs. The data demonstrated that CK-1213296 activated cardiac myosin by accelerating actin-dependent phosphate release. In cardiac myocytes, CK-1213296 increased contractility without changes in intracellular calcium, a finding consistent with its mechanism of action. In addition, CK-1213296 demonstrated an increase in cardiac contractility and stroke volume in a dog model of heart failure in a manner that supports the therapeutic hypothesis. The presentation provided non-clinical support for the Company's novel therapeutic approach of directly activating 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 clinical liabilities associated with existing pharmaceuticals. In prior presentations, Cytokinetics scientists have demonstrated that cardiac myosin activators increase cardiac contractility without stimulating beta-adrenergic receptors or inhibiting phosphodiesterase activity to increase intracellular calcium, which may be arrhythmogenic and has been associated with adverse clinical effects. Cytokinetics is planning to advance another cardiac myosin activator, CK-1827452, designated for development earlier this year, into Phase I human clinical trials for congestive heart failure in the second half of 2005. Or at least I hope so!