Ancrod in the Treatment of Acute Ischemic Stroke

Atkinson, Richard

doi:10.1159/000047500

Cited by 8 publications

(5 citation statements)

References 16 publications

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“…57 In addition, ancrod-a fibrinolytic agent derived from Malaysian pit viper venom-appears beneficial. 58 The major factor limiting the usefulness of thrombolytic therapy has been time constraints. Intravenous TPA and ancrod are effective up to 3 hours, and intra-arterial prourokinase may be effective up to 6 hours poststroke.…”

Section: Pharmacologic Intervention In the Ischemic Cascadementioning

confidence: 99%

Neuroprotection and the Ischemic Cascade

Felberg¹,

Burgin²,

Grotta³

2000

CNS spectr.

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Brain ischemia is a process of delayed neuronal cell death, not an instantaneous event. The concept of neuroprotection is based on this principle. Diminished cerebral blood flow initiates a series of events (the “ischemic cascade”) that lead to cell destruction. This ischemic cascade is akin to a spreading epidemic starting from a hypothesized core of ischemia and radiating outward. If intervention occurs early, the process may be halted.Interventions have been directed toward salvaging the ischemic penumbra. Hypothermia decreases the size of the ischemic insult in both anecdotal clinical and laboratory reports. In addition, a wide variety of agents have been shown to reduce infant volume in animal models. Pharmacologic interventions that involve thrombolysis, calcium channel blockade, and cell membrane receptor antagonism have been studied and have been found to be beneficial in animal cortical stroke models. Human trials of neuroprotective therapies have been disappointing. Other than thrombolytics, no agents, have shown an unequivocal benefit. The future of neuroprotection will require a logical extension of what has been learned in the laboratory and previous human trials. A sensible approach to the use of multiple-agent cocktails used in combination with thrombolytics is likely to offer the highest chance for benefit.

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Section: Pharmacologic Intervention In the Ischemic Cascadementioning

confidence: 99%

Neuroprotection and the Ischemic Cascade

Felberg¹,

Burgin²,

Grotta³

2000

CNS spectr.

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“…Based on the preliminary data, it appears difficult to maintain adequate plasma levels to allow for effective defibrinogenation. [2][3][4] The Phase III data have not been published and this agent is not FDA approved or available in the US.…”

Section: Ancrod Therapymentioning

confidence: 99%

“…8 An innovative treatment approach in which an attempt was made to combine initial intravenous tPA with local intraarterial thrombolysis was used in the Emergency Management of Stroke Bridging Trial. 4 This was a double-blind, randomized, placebo-controlled, multicenter feasibility study with 35 enrolled patients, in which intravenous plus intraarterial tPA (IV/IA) treatment was compared with placebo plus intraarterial tPA (placebo/IA). The study was conducted prior to the FDA approval of intravenous t-PA.…”

Section: Intraarterial Thrombolyticsmentioning

confidence: 99%

Update on therapies for acute ischemic stroke

Kindler¹,

Lopez²,

Worrall³

et al. 2000

FOC

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Acute ischemic stroke is now considered a neurological emergency for which there are new therapies. Neurosurgeons and neurologists need to remain apprised of advances in this field. The authors discuss approved and emerging therapies for patients suffering from acute ischemic stroke, based on a review of recent publications. Currently, intravenous tissue-type plasminogen activator is the only Food and Drug Administration–approved therapy for acute ischemic stroke. Intraarterial delivery of thrombolytics is a promising treatment and may be effective in selected patients. Other therapies for acute cerebral ischemia are intriguing but still in the investigational stages.

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“…Moreover, several venom enzymes, including VVSPs have proved to have potential as therapeutics for various human haemostatic disorders [11]. Despite their high sequence similarity, VVSPs differ widely in their functions.…”

Section: Introductionmentioning

confidence: 99%

Sequence and phylogenetic analysis of viper venom serine proteases

Vaiyapuri¹,

Thiyagarajan²,

Hutchinson³

et al. 2012

Bioinformation

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Abstract:Snakebites are a major neglected tropical disease responsible for as many as 95000 deaths every year worldwide. Viper venom serine proteases disrupt haemostasis of prey and victims by affecting various stages of the blood coagulation system. A better understanding of their sequence, structure, function and phylogenetic relationships will improve the knowledge on the pathological conditions and aid in the development of novel therapeutics for treating snakebites. A large dataset for all available viper venom serine proteases was developed and analysed to study various features of these enzymes. Despite the large number of venom serine protease sequences available, only a small proportion of these have been functionally characterised. Although, they share some of the common features such as a C-terminal extension, GWG motif and disulphide linkages, they vary widely between each other in features such as isoelectric points, potential N-glycosylation sites and functional characteristics. Some of the serine proteases contain substitutions for one or more of the critical residues in catalytic triad or primary specificity pockets. Phylogenetic analysis clustered all the sequences in three major groups. The sequences with substitutions in catalytic triad or specificity pocket clustered together in separate groups. Our study provides the most complete information on viper venom serine proteases to date and improves the current knowledge on the sequence, structure, function and phylogenetic relationships of these enzymes. This collective analysis of venom serine proteases will help in understanding the complexity of envenomation and potential therapeutic avenues. Background:Snakebite is a major neglected public health issue particularly among agricultural communities living in rural regions throughout the world [1, 2]. An estimated 2.5 million people are bitten by snakes each year and these are estimated to result in up to as high as 95000 deaths worldwide . Snake venom serine proteases are major components and have been identified mainly in the venoms of snakes belonging to the viperidae family with a few occurring in members of the elapidae, colubridae and hydrophidae families [8]. Many snake venom serine proteases exert their effects through the ability to disrupt the normal haemostasis of envenomed prey and victims [9]. Indeed, viper venom serine proteases (VVSPs) affect various stages of the blood coagulation system, activate platelets and directly act upon fibrinogen. These include pro-coagulant

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Ancrod in the Treatment of Acute Ischemic Stroke

Cited by 8 publications

References 16 publications

Neuroprotection and the Ischemic Cascade

Neuroprotection and the Ischemic Cascade

Update on therapies for acute ischemic stroke

Sequence and phylogenetic analysis of viper venom serine proteases

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