Replies to post #13423 on GTC Biotherapeutics (fka GTCB)

[go seek]

JL, Thank you for your post! #msg-31282373
and your investigating efforts. i.e., AT and Strokes

Human clinical trials forthcoming using AT for treatment of Strokes

Interesting, encouraging... HUGE impact on GTC if successful //
no doubt forthcoming news and publications will shine a spotlight on GTC.











The creation of a thousand forests is in one acorn.

[poorgradstudent]

>In a nutshell the cells in the oxygen deprived area send out protein messengers which trigger apoptosis (cell suicide) in the surrounding areas making the clinical condition much worse.<

Maybe this happens in the brain? I don't know because my brain physiology is horrible.

However, you need an awfully powerful microscope to find a significant amount of apoptosis in the human heart. It was all the rage for a while, but it has been shown to be virtually nonexistant (well less than 1%).

[DFRAI]

Thanks for sharing this info with us. best of luck.

[gym gravity]

jess, I'm a believer. thrombin activates par receptors and they control a bunch of downstream things. thrombin floats around in the blood and antithrombin follows it around. when things go wrong the two end up at the scene of the crime at the same time. A lot happens thereafter, some in the blood, some inside the cells. In the case of apoptosis or necrosis, or whatever osis, there is a proteolytic signal that is transmitted from the blood to the nucleus/mitochondria, across membranes.

[DewDiligence]

Is this the paper you’re referring to?

http://www.ncbi.nlm.nih.gov/pubmed/17975103

› Antithrombin Reduces Ischemic Volume, Ameliorates Neurologic Deficits, and Prolongs Animal Survival in Both Transient and Permanent Focal Ischemia

Stroke. 2007 Dec;38(12):3272-9.

Cuomo O, Pignataro G, Gala R, Scorziello A, Gravino E, Piazza O, Tufano R, Di Renzo G, Annunziato L.

Division of Pharmacology, Department of Neuroscience, School of Medicine, Federico II, University of Naples, Via S Pansini 5, 80131 Naples, Italy.

BACKGROUND AND PURPOSE: Antithrombin (AT), a glycoprotein belonging to the serpin family, blocks thrombin formation and activity at several steps. Thrombin, beside its relevant role in the coagulation cascade, exerts neurodetrimental effects through the activation of a family of protease-activated receptors, which can be implicated in stroke pathophysiology. The aims of the present study were to evaluate whether AT could reduce brain damage, ameliorate neurologic deficits, and prolong animal survival.

METHODS: Two different doses of AT (10 and 30 IU/kg IP) were administered 3 hours, 6 hours, or 3 and 6 hours after an ischemic insult to mice and rats subjected to either transient or permanent focal ischemia. Ischemic volume was evaluated 24 hours or 7 days after the ischemic insult. Neurologic deficits were also scored.

RESULTS: In mice, 10 or 30 IU/kg AT administered twice, at 3 and 6 hours after transient ischemia, and 30 IU/kg AT administered 3 hours only after transient ischemia substantially reduced total ischemic volume, significantly improved neurologic deficits evaluated 24 hours after the insult, and prolonged animal survival. In rats, the same doses given at the same time intervals significantly reduced ischemic volume, evaluated 24 hours after permanent ischemia.

CONCLUSIONS: These results indicate that AT remarkably reduces infarct volume, ameliorates neurologic deficit scores, and prolongs animal survival in 2 rodent models of brain ischemia. Taken together, our data suggest that AT, delivered via systemic administration, an easily achievable route of administration and in a clinically useful time window, could represent a new therapeutic strategy to be validated for the clinical treatment of human stroke.‹