Friday, July 28, 2006

Advances in the treatment of urge incontinence...Novel Approaches to Ventricular Fibrilation

Todays Headlines from across the DailyUpdates network
  • Breaking News (from DailyUpdates-Genitourinary Tract Disorders): Advances in the treatment of urge incontinence: BioXell’s lead molecule, Elocalcitol, is a vitamin D3 analogue that is able to prevent proliferation of both prostate and bladder tissue induced by various growth factors. Elocalcitol entered Phase IIa evaluation for the treatment of BPH in April 2003 and was found to arrest prostate growth in 92% of patients. A Phase IIb trial is currently being conducted. One of the problems associated with BPH is overactive bladder, a symptom that results from bladder hypertrophy. Thus Elocalcitol represents a promising treatment for BPH as it has the potential to reduce both prostate growth and resultant bladder hypertrophy. As well as being caused by BPH, overactive bladder can also result from the aging process or various neurological conditions and the potential market for Elocalcitol may cross multiple subtypes of overactive bladder. This market is large with 68 million people being diagnosed in the 7 principal pharmaceutical markets in 2005 (see our recent feature Dry Overactive Bladder). A segment of this patient group go on to suffer Urge Urinary Incontinence which produces a greater loss of quality of life and incurs greater costs. Over $1 billion spent on drug treatments for overactive bladder although the main approach to treating the condition involves anti-muscarinic agents despite associated tolerability issues which limit compliance. Today’s featured press release from BioXell announces plans to proceed with a Phase IIb trial of Elocalcitol in overactive bladder. The new study follows the successful completion of a Phase IIa trial of Elocalcitol in 114 women with OAB, announced in May [Source:BioXell]
  • Featured Journal Article (from DailyUpdates-Cardiovascular Disease): Novel Approaches to Ventricular Fibrilation: Ventricular fibrillation causes more than 70% of out-of-hospital cardiac arrests and is responsible for 220,000 deaths each year in the US . Our recent report Ventricular & Atrial Fibrillation report includes a detailed analysis of the causes and current treatments of this arrhythmia. The primary objectives in ventricular fibrillation patients are to restore sinus rhythm rapidly and to reduce the chance of future episodes. Electrical defibrillation remains the cornerstone in acute treatment of ventricular fibrillation. The report discusses the potassium channel, Kir6.2 and the gap junction, connexin43 as molecular targets of future pharmacological therapeutics. The peptide rotigaptide (ZP123) targets the latter by increasing junction permeability and has recently been advanced into phase 2 trials by Wyeth following its in licensing from Zealand Pharma. Today’s featured journal article reports mechanistic data for rotigaptide and in particular demonstrates that it suppressed dephosphorylation of connexin43 Ser297 and Ser368 following ischemia. These data suggest that small molecule phosphatase inhibitors could offer alternate approaches to increasing connexin43 gap junction permeability thereby offering new approaches to cardiac arrhythmia J Mol Cell Cardiol. 2006 Jun;40(6):790-8. Epub 2006 May 5.


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