CALCIUM CHANNEL BLOCKER USE AS NEUROPROTECTANT DURING STROKES
CALCIUM CHANNEL BLOCKER USE AS NEUROPROTECTANT DURING STROKES could open up a new worldwide therapeutic market valued at approximately $200 mil., according to a recent Wilkerson Group Cardiovascular Market Intelligence Service (CV/MIS) paper. Entitled "Emerging Business Opportunities in Stroke Management," the paper reports that calcium channel blockers, which already have shown some usefulness in limiting neurological damage from subarachnoid hemorrhage, may prevent neurological damage in the wider number of ischemic strokes. "Neuron death under ischemic conditions appears to be associated with the movement of calcium ions into cells and the subsequent clacium ion overload that triggers a cascade of lypolytic and proteolytic reactions within the cell," the paper explains. "If calcium channel blockers can prevent this fatal cascade reaction by stabilizing the cell membrane with regard to the movement of calcium ions, they may be able to prevent neuron death under ischemic conditions." The Wilkerson Group paper singled out three calcium channel blockers that show cerebrovascular specificity, including nimodipine (Miles' Nimotop), nifedipine (Pfizer's Procardia and Miles' Adalat), and nicardipine (Syntex' Cardene). Miles currently has an NDA pending for nimodipine for the subarachnoid hemorrhage indication. In addition to preventing the coronary artery spasm that accompanies subarachnoid hemorrhage, the calcium channel blockers' "role in increasing blood cell deformability and in preventing platelet activation" could "broaden their applications in stroke therapy," the CV/MIS paper suggests. The market potential for antiplatelet agents, including calcium channel blockers, in the stroke market is approximately $290 mil., the CV/MIS paper estimates. Other potential neuroprotectant candidates are "free radical scavengers," such as superoxide dismutase (SOD), and a class of compounds known as excitatory amino acid antagonists (EAAAs), the paper states. However, while noting the "amazing" market potential for free radical scavengers, the paper includes a word of caution. The paper lists three problems with free-radical scavengers: (1) the difficulty in establishing whether or not oxygen-free radicals cause ischemic damage; (2) the difficulty in extrapolating data from canine studies to humans; and (3) the difficulty in delivering therapeutic doses of SOD. The CV/MIS paper calls the EAAA class of compounds the "most intriguing group of neuroprotectants." The paper notes that animal studies "have shown that EAAAs can significantly diminish neuronal damage in a stroke lesion when they are administered within two to three hours after a cerebrovascular event." Merck and Nova are both working in this area of research, the paper points out. In its 1986 annual report, Nova said it has obtained patent protection "on a series of excitatory amino acid antagonists as a step forward in its work on antiepileptic drugs under grants from the National Institute of Neurologic and Communicative Diseases and Stroke." Nova indicated that it is looking initially at the group of compounds in epilepsy. Merck's lead compound in this area is MK-801; reportedly, the compound is in early clinical study. The Wilkerson Group (formerly Channing, Weinberg) is a management and strategic consulting firm based in New York that practices exclusively in the health care field. The Wilkerson Group's Cardiovascular Market Intelligence Service includes: detailed profiles of 25 cardiovascular drug and device markets worldwide; six market intelligence papers annually (the CV/MIS paper on stroke management is the third issued in 1987); and 25 hours of consultation with CV/MIS staff. The annual subscription fee is $26,000.
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