Also Wildginger... Jenni, who had such success with the drug in her case of early onset, genetic Alzheimer's was given 25 ug each week for the first 3 weeks just as compassionate use patient #3 had been.
Compassionate use trial with bryostatin A number of pre-clinical studies have implicated deficits of PKC in the etiology of AD [14, 21, 22]. Further evidence implicating PKC deficits has emerged from clinical studies that showed with autopsy-confirmation that AD patients have significant abnormalities in PKC isozymes and PKC-elicited phosphorylation of downstream substrates [15, 16, 23, 24]. Based on these studies, after the FDA allowed a compassionate use trial to proceed, patient IV-18 was treated with the potent PKC epsilon activator, bryostatin. The drug (25 micrograms/squared meter) was administered by intravenous infusion to the patient over a 1-h period once per week for the first three weeks of each month. The drug was apparently well-tolerated with no evidence of hematologic abnormalities or myalgia (the known complications of this drug which had previously been used clinically in chemotherapy regimens). More significantly, within two weeks of trial initiation, patient IV-18 showed symptomatic improvements. These included vocalizations of words, more directed attentional focus, swallowing, responses to verbal commands, and some increased range of limb motion. These improvements persisted for approximately 8 weeks, despite an episode of severe pneumonia that required intubation and hospitalization for 4 weeks. During and immediately after the episode of pneumonia, bryostatin treatment was withheld. These improvements were consistent with a previous compassionate use trial for a 95-year-old patient conducted in the Bahamas with bryostatin 3 years earlier. The current trial was conducted at intermittent intervals, with interruptions due to severe respiratory and urinary tract infections, for 5 months.
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