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Biotech / Medical : ACADIA Pharmaceuticals Inc (ACAD) -- Ignore unavailable to you. Want to Upgrade?

To: scaram(o)uche who wrote (328)	8/15/2006 12:17:00 PM
From: dr.praveen	Respond to of 588

Acadia Shares Rise on "Buy" Initiation Tuesday August 15, 11:48 am ET Acadia Pharmaceuticals Shares Get Boost From Bank of America "Buy" Coverage, Citing Pipeline NEW YORK (AP) -- Shares of biopharmaceutical company Acadia Pharmaceuticals Inc. jumped Tuesday morning after Bank Of America initiated coverage late Monday with a "Buy" rating, citing the strength of its pipeline. The stock gained 48 cents, or 8.7 percent, to $5.97 per share on the Nasdaq. Shares reached a 52-week low of $5.07 Aug. 10, marking a sharp drop from the 52-week high of $17.94 March 17. Analyst David Witzke set the 12-month target price at $10 citing what he considers five promising clinical programs. Also, the stock's decline in value and present weakness have created an attractive entry point, he said. The company focuses on developing treatments for central nervous system disorders, including schizophrenia, insomnia and Parkinson's disease. The five clinical programs focus on schizophrenia and Parkinson's treatment candidates. The markets for those treatments represent a $10 billion opportunity for the company, Witzke said in a report to investors. "Importantly, all of Acadia's development programs were internally discovered and we note that the company has five additional preclinical discovery programs, focused on glaucoma, endocrinology, sleep, neuropsychiatry, and obesity," he said. Milestones in the next 12 months include interim Phase II clinical trial data for the company's ACP-103 treatment, designed to prevent side effects of schizophrenia treatment. Also, the company is set to start two Phase II trials of ACP-103 for Parkinson's and sleep maintenance insomnia. Additionally, the company plans to start a Phase IIb trial for its anti-psychotic ACP-104, aimed at treating schizophrenia. Phase II data from a partnership with Allergen on a neuropathic pain program is also expected. Risks for the company are risks seen with many early- and mid-stage biotechnology companies. They include the early stage of development with many of its treatment candidates and the company's need for external financing, as it is currently unprofitable. Also, Witzke gives the company an "Extreme" rating for its volatility, citing the fact that it is unprofitable.

To: scaram(o)uche who wrote (328)	9/11/2006 2:14:55 PM
From: tuck	Read Replies (1) \| Respond to of 588

[Structural Requirements of Transmembrane Domain 3 for Activation by the M1 Muscarinic Receptor Agonists AC-42, AC-260584, Clozapine and N-desmethylclozapine: Evidence for three distinct modes of receptor activation] >>Mol Pharmacol. 2006 Sep 7; [Epub ahead of print] Structural Requirements of Transmembrane Domain 3 for Activation by the M1 Muscarinic Receptor Agonists AC-42, AC-260584, Clozapine and N-desmethylclozapine: Evidence for three distinct modes of receptor activation. Spalding TA, Ma JN, Ott TR, Friberg M, Bajpai A, Bradley SR, Davis RE, Brann MR, Burstein ES. Genomics Institute of the Novartis Research Foundation. Transmembrane domain three (TM3) plays a crucial role mediating muscarinic acetylcholine receptor activation by acetylcholine, carbachol, and other muscarinic agonists. We compared the effects of point mutations throughout TM3 on the interactions of carbachol, AC-42, a potent structural analogue of AC-42 called AC-260584, N-desmethylclozapine, and clozapine with the M1 muscarinic receptor. The binding and activation profiles of these ligands fell into three distinct patterns; one exemplified by orthosteric compounds like carbachol, another by structural analogs of AC-42, and a third by structural analogs of N-desmethylclozapine. All mutations tested severely reduced carbachol binding and activation of M1. In contrast, the agonist actions of AC-42 and AC-260584 were greatly potentiated by the W101A mutation, slightly reduced by Y106A and slightly increased by S109A. Clozapine and N-desmethylclozapine displayed substantially increased maximum responses at the Y106A and W101A mutants, slightly lower activity at S109A, but no substantial changes in potency. At L102A and N110A, agonist responses to AC-42, AC-260584, clozapine and N-desmethylclozapine were all substantially reduced, but usually less than carbachol. D105A showed no functional responses to all ligands. Displacement and dissociation rate experiments demonstrated clear allosteric properties of AC-42 and AC-260584, but not for N-desmethylclozapine and clozapine indicating they may contact different residues than carbachol to activate M1, but occupy substantially overlapping spaces, in contrast to AC-42 and AC-260584, which occupy separable spaces. These results show M1 receptors can be activated in at least three distinct ways and that there is no requirement for potent muscarinic agonists to mimic acetylcholine interactions with TM3.<< Full text freebie: molpharm.aspetjournals.org Cheers, Tuck

To: scaram(o)uche who wrote (328)	9/12/2006 5:27:33 PM
From: dr.praveen	Read Replies (4) \| Respond to of 588

I didn't know about this... tinyurl.com Form 8-K for ACADIA PHARMACEUTICALS INC 8-Sep-2006 Other Events Item 8.01. Other Events. On September 1, 2006, ACADIA Pharmaceuticals Inc. ("ACADIA") and the other parties to the previously disclosed civil action filed by a former employee entered into a settlement agreement. As previously disclosed, in connection with the jury verdict in this civil action, ACADIA had recorded an accrued loss from litigation totaling $9.1 million as of June 30, 2006, which included the amount awarded for damages and plaintiff's fees and costs, plus accrued interest on those awards. To fully settle the litigation inclusive of all fees and costs, pursuant to the agreement, ACADIA will make aggregate payments of $5.15 million, of which approximately $2.4 million will be covered by ACADIA's employment practices liability insurance.