Ancrod. Medical search

An enzyme fraction from the venom of the Malayan pit viper, Agkistrodon rhodostoma. It catalyzes the hydrolysis of a number of amino acid esters and a limited proteolysis of fibrinogen. It is used clinically to produce controlled defibrination in patients requiring anticoagulant therapy. EC 3.4.21.-.

A protein derived from FIBRINOGEN in the presence of THROMBIN, which forms part of the blood clot.

A generic name for film produced from wood pulp by the viscose process. It is a thin, transparent sheeting of regenerated cellulose, moisture-proof and sometimes dyed, and used chiefly as food wrapping or as bags for dialysis. (Grant & Hackh's Chemical Dictionary, 5th ed & McGraw-Hill Dictionary of Scientific and Technical Terms, 4th ed)

Plasma glycoprotein clotted by thrombin, composed of a dimer of three non-identical pairs of polypeptide chains (alpha, beta, gamma) held together by disulfide bonds. Fibrinogen clotting is a sol-gel change involving complex molecular arrangements: whereas fibrinogen is cleaved by thrombin to form polypeptides A and B, the proteolytic action of other enzymes yields different fibrinogen degradation products.

A plant genus of the family POLYGONACEAE that is used as an EDIBLE GRAIN. Although the seeds are used as cereal, the plant is not one of the cereal grasses (POACEAE).

Professional medical personnel who provide care to patients in an organized facility, institution or agency.

Behavioral response associated with the achieving of gratification.

Pathological conditions in which the BLOOD GLUCOSE cannot be maintained within the normal range, such as in HYPOGLYCEMIA and HYPERGLYCEMIA. Etiology of these disorders varies. Plasma glucose concentration is critical to survival for it is the predominant fuel for the CENTRAL NERVOUS SYSTEM.

A loose confederation of computer communication networks around the world. The networks that make up the Internet are connected through several backbone networks. The Internet grew out of the US Government ARPAnet project and was designed to facilitate information exchange.

The seventh planet in order from the sun. It is one of the five outer planets of the solar system. It has five known natural satellites.

Members of the class of compounds composed of AMINO ACIDS joined together by peptide bonds between adjacent amino acids into linear, branched or cyclical structures. OLIGOPEPTIDES are composed of approximately 2-12 amino acids. Polypeptides are composed of approximately 13 or more amino acids. PROTEINS are linear polypeptides that are normally synthesized on RIBOSOMES.

A factitious disorder characterized by habitual presentation for hospital treatment of an apparent acute illness, the patient giving a plausible and dramatic history, all of which is false.

Solutions or mixtures of toxic and nontoxic substances elaborated by snake (Ophidia) salivary glands for the purpose of killing prey or disabling predators and delivered by grooved or hollow fangs. They usually contain enzymes, toxins, and other factors.

A 60-kDa extracellular protein of Streptomyces avidinii with four high-affinity biotin binding sites. Unlike AVIDIN, streptavidin has a near neutral isoelectric point and is free of carbohydrate side chains.

A gastrointestinal peptide hormone of about 43-amino acids. It is found to be a potent stimulator of INSULIN secretion and a relatively poor inhibitor of GASTRIC ACID secretion.

The natural enzymatic dissolution of FIBRIN.

A metallocarboxypeptidase that removes C-terminal lysine and arginine from biologically active peptides and proteins thereby regulating their activity. It is a zinc enzyme with no preference shown for lysine over arginine. Pro-carboxypeptidase U in human plasma is activated by thrombin or plasmin during clotting to form the unstable carboxypeptidase U.

Works containing information articles on subjects in every field of knowledge, usually arranged in alphabetical order, or a similar work limited to a special field or subject. (From The ALA Glossary of Library and Information Science, 1983)

A single-chain polypeptide derived from bovine tissues consisting of 58 amino-acid residues. It is an inhibitor of proteolytic enzymes including CHYMOTRYPSIN; KALLIKREIN; PLASMIN; and TRYPSIN. It is used in the treatment of HEMORRHAGE associated with raised plasma concentrations of plasmin. It is also used to reduce blood loss and transfusion requirements in patients at high risk of major blood loss during and following open heart surgery with EXTRACORPOREAL CIRCULATION. (Reynolds JEF(Ed): Martindale: The Extra Pharmacopoeia (electronic version). Micromedex, Inc, Englewood, CO, 1995)

Soluble protein fragments formed by the proteolytic action of plasmin on fibrin or fibrinogen. FDP and their complexes profoundly impair the hemostatic process and are a major cause of hemorrhage in intravascular coagulation and fibrinolysis.

Use of a thrombelastograph, which provides a continuous graphic record of the physical shape of a clot during fibrin formation and subsequent lysis.

Use of marketing principles also used to sell products to consumers to promote ideas, attitudes and behaviors. Design and use of programs seeking to increase the acceptance of a social idea or practice by target groups, not for the benefit of the marketer, but to benefit the target audience and the general society.

The uncritical acceptance of an idea or plan of action.

A vitamin-K dependent zymogen present in the blood, which, upon activation by thrombin and thrombomodulin exerts anticoagulant properties by inactivating factors Va and VIIIa at the rate-limiting steps of thrombin formation.

Systemic inflammatory response syndrome with a proven or suspected infectious etiology. When sepsis is associated with organ dysfunction distant from the site of infection, it is called severe sepsis. When sepsis is accompanied by HYPOTENSION despite adequate fluid infusion, it is called SEPTIC SHOCK.

The geographic area of New England in general and when the specific state or states are not indicated. States usually included in this region are Maine, New Hampshire, Vermont, Massachusetts, Connecticut, and Rhode Island.

Technique that utilizes low-stringency polymerase chain reaction (PCR) amplification with single primers of arbitrary sequence to generate strain-specific arrays of anonymous DNA fragments. RAPD technique may be used to determine taxonomic identity, assess kinship relationships, analyze mixed genome samples, and create specific probes.

Monohydroxy derivatives of cyclohexanes that contain the general formula R-C6H11O. They have a camphorlike odor and are used in making soaps, insecticides, germicides, dry cleaning, and plasticizers.

A compound consisting of dark green crystals or crystalline powder, having a bronze-like luster. Solutions in water or alcohol have a deep blue color. Methylene blue is used as a bacteriologic stain and as an indicator. It inhibits GUANYLATE CYCLASE, and has been used to treat cyanide poisoning and to lower levels of METHEMOGLOBIN.

Mood-stimulating drugs used primarily in the treatment of affective disorders and related conditions. Several MONOAMINE OXIDASE INHIBITORS are useful as antidepressants apparently as a long-term consequence of their modulation of catecholamine levels. The tricyclic compounds useful as antidepressive agents (ANTIDEPRESSIVE AGENTS, TRICYCLIC) also appear to act through brain catecholamine systems. A third group (ANTIDEPRESSIVE AGENTS, SECOND-GENERATION) is a diverse group of drugs including some that act specifically on serotonergic systems.

A propylamine formed from the cyclization of the side chain of amphetamine. This monoamine oxidase inhibitor is effective in the treatment of major depression, dysthymic disorder, and atypical depression. It also is useful in panic and phobic disorders. (From AMA Drug Evaluations Annual, 1994, p311)

A chemically heterogeneous group of drugs that have in common the ability to block oxidative deamination of naturally occurring monoamines. (From Gilman, et al., Goodman and Gilman's The Pharmacological Basis of Therapeutics, 8th ed, p414)

A selective, irreversible inhibitor of Type B monoamine oxidase. It is used in newly diagnosed patients with Parkinson's disease. It may slow progression of the clinical disease and delay the requirement for levodopa therapy. It also may be given with levodopa upon onset of disability. (From AMA Drug Evaluations Annual, 1994, p385) The compound without isomeric designation is Deprenyl.

The absence of a useful purpose or useful result in a diagnostic procedure or therapeutic intervention. The situation of a patient whose condition will not be improved by treatment or instances in which treatment preserves permanent unconsciousness or cannot end dependence on intensive medical care. (From Ann Intern Med 1990 Jun 15;112(12):949)

A method of studying a drug or procedure in which both the subjects and investigators are kept unaware of who is actually getting which specific treatment.

A group of pathological conditions characterized by sudden, non-convulsive loss of neurological function due to BRAIN ISCHEMIA or INTRACRANIAL HEMORRHAGES. Stroke is classified by the type of tissue NECROSIS, such as the anatomic location, vasculature involved, etiology, age of the affected individual, and hemorrhagic vs. non-hemorrhagic nature. (From Adams et al., Principles of Neurology, 6th ed, pp777-810)

The systems and processes involved in the establishment, support, management, and operation of registers, e.g., disease registers.

Works about pre-planned studies of the safety, efficacy, or optimum dosage schedule (if appropriate) of one or more diagnostic, therapeutic, or prophylactic drugs, devices, or techniques selected according to predetermined criteria of eligibility and observed for predefined evidence of favorable and unfavorable effects. This concept includes clinical trials conducted both in the U.S. and in other countries.

Evaluation undertaken to assess the results or consequences of management and procedures used in combating disease in order to determine the efficacy, effectiveness, safety, and practicability of these interventions in individual cases or series.

A comprehensive radiation treatment of the entire CENTRAL NERVOUS SYSTEM.

A general term for the complete or partial loss of the ability to hear from one or both ears.

Conditions with excess LIPIDS in the blood.

Compounds that inhibit HMG-CoA reductases. They have been shown to directly lower cholesterol synthesis.

Soft tissue tumors or cancer arising from the mucosal surfaces of the LIP; oral cavity; PHARYNX; LARYNX; and cervical esophagus. Other sites included are the NOSE and PARANASAL SINUSES; SALIVARY GLANDS; THYROID GLAND and PARATHYROID GLANDS; and MELANOMA and non-melanoma skin cancers of the head and neck. (from Holland et al., Cancer Medicine, 4th ed, p1651)

An aspect of personal behavior or lifestyle, environmental exposure, or inborn or inherited characteristic, which, on the basis of epidemiologic evidence, is known to be associated with a health-related condition considered important to prevent.

Sensorineural hearing loss which develops suddenly over a period of hours or a few days. It varies in severity from mild to total deafness. Sudden deafness can be due to head trauma, vascular diseases, infections, or can appear without obvious cause or warning.

Hearing loss resulting from damage to the COCHLEA and the sensorineural elements which lie internally beyond the oval and round windows. These elements include the AUDITORY NERVE and its connections in the BRAINSTEM.

Partial or complete hearing loss in one ear.

Measurement of hearing based on the use of pure tones of various frequencies and intensities as auditory stimuli.

An oval semitransparent membrane separating the external EAR CANAL from the tympanic cavity (EAR, MIDDLE). It contains three layers: the skin of the external ear canal; the core of radially and circularly arranged collagen fibers; and the MUCOSA of the middle ear.

Development of an ischemic stroke survival score. (1/41)

BACKGROUND AND PURPOSE: There has been substantial interest in identifying predictors of survival for stroke patients. Current instruments used for measuring stroke severity are confined to either neurological, functional, or disability measures. The purpose of this study was to develop a stroke survival score that combines instruments from different domains to better predict long-term survival. METHODS: We took advantage of a particularly broad array of clinical and physiological variables collected during the Stroke Treatment with Ancrod Trial. Four hundred fifty-three patients completed a battery of instruments at day 7 after stroke and then were followed for 1 year. RESULTS: Of the 453 patients, 53% were male, 77% were aged 65 years or older, and 89% were white. One hundred nine patients (24%) died during the study period. Age was a highly significant predictor of mortality (P<0.001), but there were no statistically significant differences in 12-month survival with respect to sex, race, or educational level. The best model for predicting survival was the Ischemic Stroke Survival Score. This model included the Scandinavian Stroke Scale, Rapid Disability Rating Scale, age, and prior stroke. This model had substantially greater predictive power (R(2)=0.30, c statistic=0.86) than the Scandinavian Stroke Scale alone (R(2)=0.20, c statistic=0.78). CONCLUSIONS: This study demonstrates that combining day 7 poststroke information from multiple domains substantially improves the ability to predict 12-month survival of ischemic stroke patients compared with data from a single domain. The high mortality rate emphasizes the importance of preventive measures for a disease that has identifiable and modifiable risk factors. (+info)

Analysis of fibrin formation and proteolysis during intravenous administration of ancrod. (2/41)

Ancrod is a purified fraction of venom from the Malayan pit viper, Calloselasma rhodostoma, currently under investigation for treatment of acute ischemic stroke. Treatment with ancrod leads to fibrinogen depletion. The present study investigated the mechanisms leading to the reduction of plasma fibrinogen concentration. Twelve healthy volunteers received an intravenous infusion of 0.17 U/kg body weight of ancrod for 6 hours. Blood samples were drawn and analyzed before and at various time points until 72 hours after start of infusion. Ancrod releases fibrinopeptide A from fibrinogen, leading to the formation of desAA-fibrin monomer. In addition, a considerable proportion of desA-profibrin is formed. Production of desA-profibrin is highest at low concentrations of ancrod, whereas desA-profibrin is rapidly converted to desAA-fibrin at higher concentrations of ancrod. Both desA-profibrin and desAA-fibrin monomers form fibrin complexes. A certain proportion of complexes carries exposed fibrin polymerization sites E(A), indicating that the terminal component of the protofibril is a desAA-fibrin monomer unit. Soluble fibrin complexes potentiate tissue-type plasminogen activator-induced plasminogen activation. Significant amounts of plasmin are formed when soluble fibrin in plasma reaches a threshold concentration, leading to the proteolytic degradation of fibrinogen and fibrin. In the present setting, high concentrations of soluble fibrin are detected after 1 hour of ancrod infusion, whereas a rise in fibrinogen and fibrin degradation products, and plasmin-alpha(2)-plasmin inhibitor complex levels is first detected after 2 hours of ancrod infusion. Ancrod treatment also results in the appearance of cross-inked fibrin degradation product D-dimer in plasma. (Blood. 2000;96:2793-2802) (+info)

The effect of angrod on the delayed hypersensitivity response in rats. (3/41)

Delayed hypersensitivity was induced in rats by means of sheep erythrocytes and bovine serum albumin-lipid conjugate. Administration of heparin to rats sensitized to either antigen resulted in diminution of the delayed hypersensitivity reaction. Administration of ancrod, however, failed to inhibit the delayed cellular reaction to either antigen. Granuloma formation remained unaffected when rats were injected with either heparin or ancrod. The lack of ancrod effect, in contrast to heparin effect, on delayed hypersensitivity is discussed. (+info)

A quantitative evaluation of anticoagulants in experimental nephrotoxic nephritis. (4/41)

The protective effects of anticoagulants in nephrotoxic nephritis in rabbits have been studied, using various doses of heparin and defibrination with ancrod. Massive doses of heparin (2000 units/kg/day) were required before significant reduction in glomerular fibrin deposition, extracepillary cell proliferation and urea retention occurred. Doses of 300 and 1000 units/kg/day were insufficient to modify fibrin deposition and cell proliferation. Defibrination with ancrod provided protection, judged by histological and functional criteria, comparable to 2000 units of heparin/kg/day; but fibrin could still be demonstrated in the glomeruli of animals treated with 2000 units of heparin/kg/day, contrasting with the virtual absence of fibrin in animals given ancrod. (+info)

The effects of defibrination with ancrod in experimental allergic glomerular injury. (5/41)

Quantitative studies of the effects of defibrination (with ancrod) have been undertaken in two forms of allergic glomerular damage, nephrotoxic serum nephritis and acute serum sickness in rabbits. No differences in intrarenal fixation of nephrotoxic antibody, complement activation or host antibody response were detected between defibrinated and untreated rabbits with nephrotoxic serum nephritis. Defibrination prevented intraglomerular fibrin deposition in this disease; but some glomerular damage as shown by a rise in blood urea and endothelial proliferation still occurred in defibrinated animals. No differences in immune elimination of BSA, circulating immune complex formation or intrarenal localization of immune complexes were noted in defibrinated animals with acute serum sickness. No intraglomerular fibrin deposition was detected in treated or untreated animals in this disease model. It is concluded that the protective effects of ancrod are directly related to defibrination, and not to any other modification of allergic events. (+info)

Fibrinogen depletion attenuates Staphyloccocus aureus infection by preventing density-dependent virulence gene up-regulation. (6/41)

Staphylococcus aureus undergoes a density-dependent conversion in phenotype from tissue-adhering to tissue-damaging and phagocyte-evading that is mediated in part by the quorum-sensing operon, agr, and its effector, RNAIII. Contributions of host factors to this mechanism for regulating virulence have not been studied. We hypothesized that fibrinogen, as a component of the inflammatory response, could create spatially constrained microenvironments around bacteria that increase density independently of bacterial numbers and thus potentiate quorum-sensing-dependent virulence gene expression. Here we show that transient fibrinogen depletion significantly reduces the bacterial burden and the consequential morbidity and mortality during experimental infection with wild-type S. aureus, but not with bacteria that lack expression of the quorum-sensing operon, agr. In addition, it inhibits in vivo activation of the promoter for the agr effector, RNAIII, and downstream targets of RNAIII, including alpha hemolysin and capsule production. Moreover, both in vitro and in vivo, the mechanism for promoting this phenotypic switch in virulence involves clumping of the bacteria, demonstrating that S. aureus responds to fibrinogen-mediated bacterial clumping by enhancing density-dependent virulence gene expression. These data demonstrate that down-modulation of specific inflammatory components of the host that augment bacterial quorum sensing can be a strategy for enhancing host defense against infection. (+info)

Embolization itself stimulates thrombus propagation in pulmonary embolism. (7/41)

The role of active thrombosis in the pathophysiology of pulmonary embolism is unclear. We tested the hypothesis that venous thrombi significantly increase their thrombotic activity once they embolize into the high-flow circulation of the pulmonary arteries. Thrombotic activity was measured using an immunoassay that measures both fibrinopeptide B (FPB) as well as its most abundant metabolite des-arginine FPB. Thrombi were formed in the femoral veins of adult dogs. In one group, the thrombi were embolized without anticoagulation. In the second group, heparin (300 U/kg bolus, then 90 U x kg(-1) x h(-1) infusion) was administered before embolization to prevent subsequent thrombotic activity. Plasma FPB concentrations were significantly suppressed in the heparinized group relative to the nonheparinized group for 1 h postembolization (P = 0.038). We conclude that pulmonary embolization itself causes preexisting venous thrombi to greatly intensify their thrombotic activity and that embolization-associated thrombus propagation can be prevented by heparin. (+info)

Soluble fibrin is the main mediator of Staphylococcus aureus adhesion to platelets. (8/41)

BACKGROUND: Infective endocarditis (IE) caused by Staphylococcus aureus is associated with significant morbidity and mortality rates. Platelets play a dual role as adhesive cells forming associates with bacteria as well as specialized inflammatory cells. The specific role of the various factors involved in bacteria-platelet association has not yet been fully elucidated. METHODS AND RESULTS: We observed a dramatic increase in the capability to bind S aureus when platelets were activated with thrombin (from 5% to 30%, P<0.001). To pinpoint platelet-binding sites involved in the interaction, platelets from knockout mice and from patients with selective inherited deficiency of membrane proteins or of granules were used. CD36, GPIIb/IIIa, and P-selectin were excluded as receptors for S aureus. Platelets from patients with alpha-delta-storage pool disease and Gray platelet syndrome indicate the requirement of alpha-granule contents. Platelet activation by ADP did not promote platelet-S aureus associate formation, although these platelets were covered with bound fibrinogen. Only small numbers of associates between fibrinogen-covered bacteria and ADP-activated platelets were observed. Formation of fibrin alone was also not sufficient to induce association. Only when fibrin formation and platelet activation occurred together were large numbers of associates formed (P<0.001). A potential receptor for fibrin on S aureus is clumping factor A. Addition of thrombospondin-1 to control platelets increased the number of associates (P=0.02). CONCLUSIONS: Soluble fibrin but not fibrinogen is the main mediator of platelet-S aureus association. In addition, platelet activation and the release of alpha-granule contents, particularly thrombospondin-1, is a requirement for platelet-S aureus association. (+info)

... the German company that had discovered and started developing ancrod, and had acquired the rights to ancrod in 2002, after ... Ancrod became NTI's lead product; in 2006 Frieman estimated annual sales $500 million to $1 billion. The company collapsed when ... In 2004 NTI acquired Empire Pharmaceuticals, which had one product: ancrod (Viprinex). Empire had been formed by former ... the company was dissolved in 2009 after the failure of its drug candidate ancrod in a Phase III trial for ischemic stroke. The ...

https://en.wikipedia.org/wiki/Neurobiological_Technologies

Multiple courses of ancrod (Arvin) therapy. Br Med J 1977; 1(6056): 290-1. Kounis NG, Evans WH. Treatment of chronic ...

https://en.wikipedia.org/wiki/Nicholas_Kounis

When plasmin breaks down fibrin, a number of soluble parts are produced. These are called fibrin degradation products (FDPs). FDPs compete with thrombin, and thus slow down clot formation by preventing the conversion of fibrinogen to fibrin. This effect can be seen in the thrombin clotting time (TCT) test, which is prolonged in a person that has active fibrinolysis.. FDPs, and a specific FDP, the D-dimer, can be measured using antibody-antigen technology. This is more specific than the TCT, and confirms that fibrinolysis has occurred. It is therefore used to indicate deep-vein thrombosis, pulmonary embolism, DIC and efficacy of treatment in acute myocardial infarction. Alternatively, a more rapid detection of fibrinolytic activity, especially hyperfibrinolysis, is possible with thromboelastometry (TEM) in whole blood, even in patients on heparin. In this assay, increased fibrinolysis is assessed by comparing the TEM profile in the absence or presence of the fibrinolysis inhibitor aprotinin. ...

https://en.wikipedia.org/wiki/Fibrinolysis

In 2001, Eli Lilly's chairman, president and CEO, Sidney Taurel, told shareholders: "No medicine better symbolizes our mission than Xigris," calling it "one of our industry's genuine breakthroughs."[5]. Xigris was designed to fight sepsis, a condition that kills more than 200,000 Americans annually. It was the only approved drug for sepsis, and it costs $8,000 to treat a single patient. Lilly hoped it would be a blockbuster, with sales of at least a billion dollars a year. But after five years on the market, sales were only $200 million.. Eli Lilly used the Belsito & Company PR firm in a marketing campaign to promote Xigris, its drug for treatment of sepsis. A report in the New England Journal of Medicine (NEJM) accused the company of initiating false reports of a shortage of the drug to boost sales.[6] Belsito and Company spread the word that the drug was being "rationed" and physicians were being 'systematically forced' to decide who would live and who would die. As part of this effort, Lilly ...

https://en.wikipedia.org/wiki/Drotrecogin_alfa

Acetylsalicylic acid is a weak acid, and very little of it is ionized in the stomach after oral administration. Acetylsalicylic acid is quickly absorbed through the cell membrane in the acidic conditions of the stomach. The increased pH and larger surface area of the small intestine causes aspirin to be absorbed more slowly there, as more of it is ionised. Owing to the formation of concretions, aspirin is absorbed much more slowly during overdose, and plasma concentrations can continue to rise for up to 24 hours after ingestion.[152][153][154] About 50-80% of salicylate in the blood is bound to albumin protein, while the rest remains in the active, ionized state; protein binding is concentration-dependent. Saturation of binding sites leads to more free salicylate and increased toxicity. The volume of distribution is 0.1-0.2 L/kg. Acidosis increases the volume of distribution because of enhancement of tissue penetration of salicylates.[154] As much as 80% of therapeutic doses of salicylic acid is ...

https://en.wikipedia.org/wiki/Acetylsalicylic_acid

These drugs deplete the active form of the vitamin by inhibiting the enzyme vitamin K epoxide reductase and thus the recycling of the inactive vitamin K epoxide back to the active reduced form of vitamin K. The drugs are structurally similar to vitamin K and act as competitive inhibitors of the enzyme. The term "vitamin K antagonist" is a misnomer, as the drugs do not directly antagonise the action of vitamin K in the pharmacological sense, but rather the recycling of vitamin K. Vitamin K is required for the proper production of certain proteins involved in the blood clotting process. For example, it is needed to carboxylate specific glutamic acid residues on prothrombin. Without these residues carboxylated, the protein will not form the appropriate conformation of thrombin, which is needed to produce the fibrin monomers that are polymerized to form clots.[1] The action of this class of anticoagulants may be reversed by administering vitamin K for the duration of the anticoagulant's residence in ...

https://en.wikipedia.org/wiki/Vitamin_K_antagonist

The drug is clear with a pH of 10.[7] Its production is inhibited indirectly by NSAIDs, which inhibit the cyclooxygenase enzymes COX1 and COX2. These convert arachidonic acid to prostaglandin H2 (PGH2), the immediate precursor of prostacyclin. Since thromboxane (an eicosanoid stimulator of platelet aggregation) is also downstream of COX enzymes, one might think that the effect of NSAIDs would act to balance. However, prostacyclin concentrations recover much faster than thromboxane levels, so aspirin administration initially has little to no effect but eventually prevents platelet aggregation (the effect of prostaglandins predominates as they are regenerated). This is explained by understanding the cells that produce each molecule, TXA2 and PGI2. Since PGI2 is primarily produced in a nucleated endothelial cell, the COX inhibition by NSAID can be overcome with time by increased COX gene activation and subsequent production of more COX enzymes to catalyze the formation of PGI2. In contrast, TXA2 is ...

https://en.wikipedia.org/wiki/Prostacyclin

... (Ro 48-3657, proposed brand name Xubix) is the double prodrug of Ro-44-3888, which is a platelet aggregation inhibitor. It was being developed for secondary prevention of arterial thrombosis following unstable angina pectoris and acute myocardial infarction (MI). On August 6, 1999, Hoffmann-La Roche announced that the preliminary results from Phase III clinical trials had not shown that sibrafiban was better than aspirin in preventing recurrent ischemic events in patients suffering from acute coronary syndrome. The development of sibrafiban was terminated. ...

https://en.wikipedia.org/wiki/Sibrafiban

In industry, EDTA is mainly used to sequester metal ions in aqueous solution. In the textile industry, it prevents metal ion impurities from modifying colors of dyed products. In the pulp and paper industry, EDTA inhibits the ability of metal ions, especially Mn2+, from catalyzing the disproportionation of hydrogen peroxide, which is used in chlorine-free bleaching. In a similar manner, EDTA is added to some food as a preservative or stabilizer to prevent catalytic oxidative decoloration, which is catalyzed by metal ions.[4] In soft drinks containing ascorbic acid and sodium benzoate, EDTA mitigates formation of benzene (a carcinogen).[5] The reduction of water hardness in laundry applications and the dissolution of scale in boilers both rely on EDTA and related complexants to bind Ca2+, Mg2+, as well as other metal ions. Once bound to EDTA, these metal centers tend not to form precipitates or to interfere with the action of the soaps and detergents. For similar reasons, cleaning solutions often ...

https://en.wikipedia.org/wiki/Edta

As of March 2017, brands included Aclop, Actaclo, Agregex, Agrelan, Agrelax, Agreless, Agrelex, Agreplat, Anclog, Angiclod, Anplat, Antiagrex, Antiban, Antigrel, Antiplaq, Antiplar, Aplate, Apolets, Areplex, Artepid, Asogrel, Atelit, Atelit, Ateplax, Atervix, Atheros, Athorel, Atrombin, Attera, Bidogrel, Bigrel, Borgavix, Carder, Cardogrel, Carpigrel, Ceraenade, Ceruvin, Cidorix, Clatex, Clavix, Clentel, Clentel, Clidorel, Clodel, Clodelib, Clodian, Clodil, Cloflow, Clofre, Clogan, Clogin, Clognil, Clogrel, Clogrelhexal, Clolyse, Clont, Clood, Clopacin, Clopcare, Clopeno, Clopex Agrel, Clopez, Clopi, Clopid, Clopida, Clopidep, Clopidexcel, Clopidix, Clopidogrel, Clopidogrelum, Clopidomed, Clopidorex, Clopidosyn, Clopidoteg, Clopidowel, Clopidra, Clopidrax, Clopidrol, Clopigal, Clopigamma, Clopigrel, Clopilet, Clopimed, Clopimef, Clopimet, Clopinovo, Clopione, Clopiright, Clopirite, Clopirod, Clopisan, Clopistad, Clopistad, Clopitab, Clopithan, Clopitro, ClopiVale, Clopivas, Clopivaz, Clopivid, ...

https://en.wikipedia.org/wiki/Plavix

B01AD09 Ancrod. B01AD10 Drotrecogin alfa (activated). B01AD11 Tenecteplase. B01AD12 Protein C. B01AE Direct thrombin inhibitors ...

https://en.wikipedia.org/wiki/ATC_code_B01

Examples include ancrod and batroxobin, two serine proteases from snakes that have been used in medical preparations. Venombin ... Kelton, JG; Smith, JW; Moffatt, D; Santos, A; Horsewood, P (1999). "The interaction of ancrod with human platelets". Platelets ... Nolan C, Hall LS, Barlow GH (1976). "Ancrod, the coagulating enzyme from Malayan pit viper (Agkistrodon rhodostoma) venom". ... ancrod) is an enzyme. This enzyme catalyses the following chemical reaction Selective cleavage of Arg- bond in fibrinogen, to ...

https://en.wikipedia.org/wiki/Venombin_A

Ancrod, another medical snake venom serine protease Bruck H, Salem G (June 1954). "[Reptilase, a hemostatic for prophylaxis and ...

https://en.wikipedia.org/wiki/Batroxobin

The venom of this species is used to isolate a thrombin-like enzyme called ancrod. This enzyme is used clinically to break down ... "Molecular cloning and sequence analysis of the cDNA for ancrod, a thrombin-like enzyme from the venom of Calloselasma ...

https://en.wikipedia.org/wiki/Calloselasma

Ancrod (also known as Viprinex), a serine protease derived from the venom of the Malayan pit vipers, was under development for ... In 2004 Empire was acquired by Neurobiological Technologies (NTI). Ancrod failed in a Phase III clinical trial in 2008, which ... a startup that included a Knoll employee who had worked on ancrod. ... the treatment of acute ischemic stroke; after Knoll was acquired by Abbott, Abbott licensed the rights to ancrod to Empire ...

https://en.wikipedia.org/wiki/Knoll_Pharmaceuticals

... ancrod (INN) andolast (INN) Andriol Androcur Androderm Androgel Android-f Android Androlone androstanolone (INN) Anectine ...

https://en.wikipedia.org/wiki/List_of_drugs:_An–Ap

... ancrod MeSH D08.811.277.656.300.760.955.135 - batroxobin MeSH D08.811.277.656.300.775 - streptokinase MeSH D08.811.277.656. ...

https://en.wikipedia.org/wiki/List_of_MeSH_codes_(D08)

... ancrod MeSH D20.888.850.960.200.105 - batroxobin MeSH D20.888.850.960.200.210 - crotoxin MeSH D20.944.380 - hazardous waste ...

https://en.wikipedia.org/wiki/List_of_MeSH_codes_(D20)

... ancrod MeSH D23.946.833.850.960.200.105 - batroxobin MeSH D23.946.833.850.960.200.210 - crotoxin MeSH D23.946.896.980 - ...

https://en.wikipedia.org/wiki/List_of_MeSH_codes_(D23)

... is not approved or marketed in any country. It is a thrombin-like serine protease. As of 2017 ancrod was not marketed ... Ancrod has a triple mode of action. It was found that ancrod's actions are FAD dependent and that the substance has interesting ... Finally, ancrod decreases the likelihood of local thrombotic events. These mechanisms also account for ancrod's activity in ... "Ancrod for the treatment of acute ischemic brain infarction. The Ancrod Stroke Study Investigators". Stroke. 25 (9): 1755-9. ...

https://en.wikipedia.org/wiki/Ancrod

... a is the activated form of the coagulation factor thrombokinase, known eponymously as Stuart-Prower factor. Factor X is an enzyme, a serine endopeptidase, which plays a key role at several stages of the coagulation system. Factor X is synthesized in the liver. The most commonly used anticoagulants in clinical practice, warfarin and the heparin series of anticoagulants and fondaparinux, act to inhibit the action of Factor Xa in various degrees. Traditional models of coagulation developed in the 1960s envisaged two separate cascades, the extrinsic (tissue factor (TF)) pathway and the intrinsic pathway. These pathways converge to a common point, the formation of the Factor Xa/Va complex which together with calcium and bound on a phospholipids surface generate thrombin (Factor IIa) from prothrombin (Factor II). A new model, the cell-based model of anticoagulation appears to explain more fully the steps in coagulation. This model has three stages: 1) initiation of coagulation on TF-bearing ...

https://en.wikipedia.org/wiki/Factor_X

Symptoms of mild cinchonism (which may occur from standard therapeutic doses of quinine) include flushed and sweaty skin, ringing of the ears (tinnitus), blurred vision, impaired hearing, confusion, reversible high-frequency hearing loss, headache, abdominal pain, rashes, drug-induced lichenoid reaction (lichenoid photosensitivity),[1] vertigo, dizziness, dysphoria, nausea, vomiting and diarrhea. Large doses of quinine may lead to severe (but reversible) symptoms of cinchonism: skin rashes, deafness, somnolence, diminished visual acuity or blindness, anaphylactic shock, and disturbances in heart rhythm or conduction, and death from cardiotoxicity (damage to the heart). Quinine may also trigger a rare form of hypersensitivity reaction in malaria patients, termed blackwater fever, that results in massive hemolysis, hemoglobinemia, hemoglobinuria, and kidney failure.[citation needed] Most symptoms of cinchonism (except in severe cases) are reversible and disappear once quinine is withdrawn. ...

https://en.wikipedia.org/wiki/Cinchonism

Luo C, Thielens NM, Gagnon J, Gal P, Sarvari M, Tseng Y, Tosi M, Zavodszky P, Arlaud GJ, Schumaker VN (May 1992). "Recombinant human complement subcomponent C1s lacking beta-hydroxyasparagine, sialic acid, and one of its two carbohydrate chains still reassembles with C1q and C1r to form a functional C1 complex". Biochemistry. 31 (17): 4254-62. doi:10.1021/bi00132a015. PMID 1533159 ...

https://en.wikipedia.org/wiki/Complement_component_1s

In other less formal contexts, an alcohol is often called with the name of the corresponding alkyl group followed by the word "alcohol", e.g., methyl alcohol, ethyl alcohol. Propyl alcohol may be n-propyl alcohol or isopropyl alcohol, depending on whether the hydroxyl group is bonded to the end or middle carbon on the straight propane chain. As described under systematic naming, if another group on the molecule takes priority, the alcohol moiety is often indicated using the "hydroxy-" prefix.[17] Alcohols are then classified into primary, secondary (sec-, s-), and tertiary (tert-, t-), based upon the number of carbon atoms connected to the carbon atom that bears the hydroxyl functional group. (The respective numeric shorthands 1°, 2°, and 3° are also sometimes used in informal settings.[18]) The primary alcohols have general formulas RCH2OH. The simplest primary alcohol is methanol (CH3OH), for which R=H, and the next is ethanol, for which R=CH3, the methyl group. Secondary alcohols are those ...

https://en.wikipedia.org/wiki/Alcohol

... is a condition or a process in which an organism becomes chemically harmed severely (poisoned) by a toxic substance or venom of an animal.[1] Acute poisoning is exposure to a poison on one occasion or during a short period of time. Symptoms develop in close relation to the degree of exposure. Absorption of a poison is necessary for systemic poisoning (that is, in the blood throughout the body). In contrast, substances that destroy tissue but do not absorb, such as lye, are classified as corrosives rather than poisons. Furthermore, many common household medications are not labeled with skull and crossbones, although they can cause severe illness or even death. In the medical sense, toxicity and poisoning can be caused by less dangerous substances than those legally classified as a poison. Toxicology is the study and practice of the symptoms, mechanisms, diagnosis, and treatment of poisoning. Chronic poisoning is long-term repeated or continuous exposure to a poison where symptoms do not ...

https://en.wikipedia.org/wiki/Poisoning

... can be measured by its effects on the target (organism, organ, tissue or cell). Because individuals typically have different levels of response to the same dose of a toxic substance, a population-level measure of toxicity is often used which relates the probabilities of an outcome for a given individual in a population. One such measure is the LD50. When such data does not exist, estimates are made by comparison to known similar toxic things, or to similar exposures in similar organisms. Then, "safety factors" are added to account for uncertainties in data and evaluation processes. For example, if a dose of a toxic substance is safe for a laboratory rat, one might assume that one tenth that dose would be safe for a human, allowing a safety factor of 10 to allow for interspecies differences between two mammals; if the data are from fish, one might use a factor of 100 to account for the greater difference between two chordate classes (fish and mammals). Similarly, an extra protection ...

https://en.wikipedia.org/wiki/Toxic_effect

More than 64,000 Americans died from drug overdoses in 2016.[1] Since 2000, the US drug overdose death rate has gone from 6.2 per 100,000 people in 2000 to 14.7 per 100,000 in 2014.[17] The National Center for Health Statistics report that 19,250 people died of accidental poisoning in the U.S. in the year 2004 (8 deaths per 100,000 population).[18] In 2008 testimony before a Senate subcommittee, Leonard J. Paulozzi,[19] a medical epidemiologist at the Centers for Disease Control and Prevention stated that in 2005 more than 22,000 American lives were lost due to overdoses, and the number is growing rapidly. Paulozzi also testified that all available evidence suggests that unintentional overdose deaths are related to the increasing use of prescription drugs, especially opioid painkillers.[20] However, the vast majority of overdoses are also attributable to alcohol. It is very rare for a victim of an overdose to have consumed just one drug. Most overdoses occur when drugs are ingested in ...

https://en.wikipedia.org/wiki/Overdose

Protein HtrA2, also known as Omi, is a mitochondrially-located serine protease. The human protein Serine protease HTRA2, mitochondrial is 49kDa in size and composed of 458 amino acids. The peptide fragment of 1-31 amino acid is the mitochondrial transition sequence, fragment 32-133 amino acid is propertied, and 134-458 is the mature protein Serine protease HTRA2, mitochondrial, and its theoretical pI of this protein is 6.12.[10] HtrA2 shows similarities with DegS, a bacterial protease present in the periplasm of gram-negative bacteria. Structurally, HtrA2 is a trimeric molecule with central protease domains and a carboxy-terminal PDZ domain, which is characteristic of the HtrA family. The PDZ domain preferentially binds C-terminus of the protein substrate and modulate the proteolytic activity of the trypsin-like protease domain.[11] ...

https://en.wikipedia.org/wiki/HtrA_serine_peptidase_2

In biology, poisons are substances that cause disturbances in organisms, usually by chemical reaction or other activity on the molecular scale, when an organism absorbs a sufficient quantity.[1][2] The fields of medicine (particularly veterinary) and zoology often distinguish a poison from a toxin, and from a venom. Toxins are poisons produced by organisms in nature, and venoms are toxins injected by a bite or sting (this is exclusive to animals). The difference between venom and other poisons is the delivery method. Industry, agriculture, and other sectors employ poisonous substances for reasons other than their toxicity. Most poisonous industrial compounds have associated material safety data sheets and are classed as hazardous substances. Hazardous substances are subject to extensive regulation on production, procurement and use in overlapping domains of occupational safety and health, public health, drinking water quality standards, air pollution and environmental protection. Due to the ...

https://en.wikipedia.org/wiki/Poisonous

Ancrod is not approved or marketed in any country. It is a thrombin-like serine protease. As of 2017 ancrod was not marketed ... Ancrod has a triple mode of action. It was found that ancrods actions are FAD dependent and that the substance has interesting ... Finally, ancrod decreases the likelihood of local thrombotic events. These mechanisms also account for ancrods activity in ... "Ancrod for the treatment of acute ischemic brain infarction. The Ancrod Stroke Study Investigators". Stroke. 25 (9): 1755-9. ...

https://en.wikipedia.org/wiki/Ancrod

In rabbits with nephrotoxic nephritis, defibrination with ancrod provided protection when administered during the autologous ... Defibrination with ancrod in nephrotoxic nephritis in rabbits. ... Defibrination with ancrod in nephrotoxic nephritis in rabbits ... Defibrination with ancrod in nephrotoxic nephritis in rabbits. In rabbits with nephrotoxic nephritis, defibrination with ancrod ...

https://pubmed.ncbi.nlm.nih.gov/794557/?dopt=Abstract

PubMed journal article Cardiopulmonary bypass with danaparoid sodium and ancrod in heparin-induced thrombocytopeni were found ... AncrodAnticoagulantsAortic Valve StenosisCardiopulmonary BypassChondroitin SulfatesCoronary DiseaseDermatan SulfateDrug ... We discuss the reasons for this and suggest that the combination of ancrod and danaparoid sodium is a logical one in such cases ... "Cardiopulmonary Bypass With Danaparoid Sodium and Ancrod in Heparin-induced Thrombocytopenia." The Annals of Thoracic Surgery, ...

https://www.unboundmedicine.com/medline/citation/9725413/Cardiopulmonary_bypass_with_danaparoid_sodium_and_ancrod_in_heparin_induced_thrombocytopenia_

Efficacy, Safety, and Tolerability of Ancrod in Patients With Sudden Hearing Loss. The safety and scientific validity of this ... The purpose of this study is to determine whether ancrod is effective and safe in the treatment of sudden sensorineural hearing ... Ancrod. Anticoagulants. Fibrinolytic Agents. Fibrin Modulating Agents. Molecular Mechanisms of Pharmacological Action. ... Double-blind, Randomized, Placebo-controlled Study on Efficacy, Safety and Tolerability of Ancrod in Patients With Sudden ...

https://clinicaltrials.gov/ct2/show/NCT01621256?recr=Open&cond=%22Ear+Diseases%22&rank=4

Subcutaneous Ancrod Therapy in Peripheral Arterial Disease: Improvement in Blood Viscosity and Nutritional Blood Flow G. D. O. ... G. D. O. Lowe, J. J. Morrice, C. D. Forbes, C. R. M. Prentice, J. C. Barbenel; Subcutaneous Ancrod Therapy in Peripheral ... Molecular cloning and sequence analysis of the cDNA for ancrod, a thrombin-like enzyme from the venom of Calloselasma ...

https://portlandpress.com/clinsci/article-abstract/52/2/1P/73188/Subcutaneous-Ancrod-Therapy-in-Peripheral-Arterial

We use cookies to enhance your experience on our website. By continuing to use our website, you are agreeing to our use of cookies. You can change your cookie settings at any time.Find out more ...

http://oxfordindex.oup.com/view/10.1093/oi/authority.20110810104345923

... , how to boost immune system fight off hpv, pt 141 bremelanotide peptide yy, glucagen hypokit ...

http://buysemax.com/ancrod-snake-venom-peptide.html

The physicochemical properties evaluation of ancrod and nimesulide are formally summarized in table 1. I cant help us but feel ... Ancrod by teva pharmaceuticals usa inc. January 31, 2020 Joseph Medical No Comments Magnesium aluminum hydroxide, commonly ... The physicochemical properties evaluation of ancrod and nimesulide are formally summarized in table 1. ...

https://goebel5.org/ancrod-by-teva-pharmaceuticals-usa-inc/

https://en.wikipedia.org/wiki/Fibrinolysis

In 2001, Eli Lillys chairman, president and CEO, Sidney Taurel, told shareholders: "No medicine better symbolizes our mission than Xigris," calling it "one of our industrys genuine breakthroughs."[5]. Xigris was designed to fight sepsis, a condition that kills more than 200,000 Americans annually. It was the only approved drug for sepsis, and it costs $8,000 to treat a single patient. Lilly hoped it would be a blockbuster, with sales of at least a billion dollars a year. But after five years on the market, sales were only $200 million.. Eli Lilly used the Belsito & Company PR firm in a marketing campaign to promote Xigris, its drug for treatment of sepsis. A report in the New England Journal of Medicine (NEJM) accused the company of initiating false reports of a shortage of the drug to boost sales.[6] Belsito and Company spread the word that the drug was being "rationed" and physicians were being systematically forced to decide who would live and who would die. As part of this effort, Lilly ...

https://en.wikipedia.org/wiki/Drotrecogin_alfa

Ancrod (Viprinex®)Drug Intervention Desc:. Fibrinogenolytic agent. Purified fraction of pit viper venom, cleaves fibrinogen.. ... Patients were treated with either low-molecular weight dextran and mannitol alone (group A) or in combination with ancrod ( ...

http://www.strokecenter.org/trials/clinicalstudies/controlled-trial-of-ancrod-in-ischemic-stroke/description

Viprinex (Ancrod). VIPRINEX® Knoll Ancrod Anticoagulant Action And Clinical Pharmacology: Ancrod, a thrombin-like enzyme ...

https://www.rxmed.com/illness/priapism

Detailed drug Information for Deconamine SR. Includes common brand names, drug descriptions, warnings, side effects and dosing information.

https://www.drugs.com/cons/deconamine-sr.html

Do not take desvenlafaxine with a monoamine oxidase (MAO) inhibitor (eg, isocarboxazid [Marplan®], linezolid (Zyvox®), methylene blue injection, phenelzine [Nardil®], selegiline [Eldepryl®], tranylcypromine [Parnate®]). Do not start taking desvenlafaxine during the 2 weeks after you stop a MAO inhibitor and wait 1 week after stopping desvenlafaxine before you start taking a MAO inhibitor. If you take them together or do not wait the proper amount of time, you may develop confusion, agitation, restlessness, stomach or intestinal symptoms, a sudden high body temperature, an extremely high blood pressure, or severe convulsions. Do not take any medicine that contains venlafaxine (Effexor®) while you are using Khedezla® or Pristiq®. Desvenlafaxine may cause some teenagers and young adults to be agitated, irritable, or display other abnormal behaviors. It may also cause some people to have suicidal thoughts and tendencies or to become more depressed. Some people may have trouble sleeping, get ...

https://www.mayoclinic.org/drugs-supplements/desvenlafaxine-oral-route/before-using/drg-20071583?p=1

Do not take thioridazine (Mellaril®) with fluoxetine and wait 5 weeks after stopping fluoxetine before you start taking thioridazine. Do not use pimozide (Orap®) with fluoxetine. Using these medicines together can cause very serious heart problems. Fluoxetine may cause a serious condition called serotonin syndrome if taken together with some medicines. Do not use fluoxetine with buspirone (Buspar®), fentanyl (Abstral®, Duragesic®), lithium (Eskalith®, Lithobid®), tryptophan, St. Johns wort, amphetamines, or some pain or migraine medicines (eg, rizatriptan, sumatriptan, tramadol, Frova®, Imitrex®, Maxalt®, Relpax®, Ultram®, Zomig®). Check with your doctor first before taking any other medicines with fluoxetine. Fluoxetine may cause some teenagers and young adults to be agitated, irritable, or display other abnormal behaviors. It may also cause some people to have suicidal thoughts and tendencies or to become more depressed. Some people may have trouble sleeping, get upset easily, ...

https://www.mayoclinic.org/drugs-supplements/fluoxetine-oral-route/before-using/drg-20063952?p=1

Label: Intravenous ancrod. Description: Intravenous ancrod infused at a rate of 0.167 IU/kg/hr (0.6 mL/kg/hr) for 2 or 3 hours ... National Institute of Health Stroke Scale (NIHSS),Barthel Index (BI),Fibrinogen levels with ancrod tx, and Safety of ancrod tx ... Ancrod (Viprinex) Biological Intervention Desc:. 0.167 IU/kg/hr (0.6 mL/kg/hr) IV for 2-3 hours. ... Ancrod (Viprinex®)Drug Intervention Desc:. Fibrinogenolytic agent. Purified fraction of pit viper venom, cleaves fibrinogen.. ...

http://www.strokecenter.org/trials/clinicalstudies/ancrod-viprinex%E2%84%A2-for-the-treatment-of-acute-ischemic-stroke/description

Efficacy, Safety, and Tolerability of Ancrod in Patients With Sudden Hearing Loss. *Hearing Loss ...

https://clinicaltrials.gov/ct2/results?recr=Open&cond=%22Hearing+Disorders%22&show_rss=Y

Ancrod 3.4.21.28. Angiotensin Converting Enzyme - HPLC Stopped Analysis 3.4.15.1. Angiotensin Converting Enzyme - ...

https://www.sigmaaldrich.com/life-science/metabolomics/enzyme-explorer/learning-center/assay-library.html

This study is investigating the efficacy and safety of ancrod [NM-V, Viprinex; Nordmark Arzneimittel] in patients with sudden ... Double-blind, Randomized, Placebo-controlled Study on Efficacy, Safety and Tolerability of Ancrod in Patients With Sudden ... Double-blind, Randomized, Placebo-controlled Study on Efficacy, Safety and Tolerability of Ancrod in Patients With Sudden ...

http://adisinsight.springer.com/trials/700245511?error=cookies_not_supported&code=2eb22396-17b4-4bcf-a13c-aedd7f8d4ab4

Study Cardio-Pulmonary Bypass flashcards from Cindy Ehret

https://www.brainscape.com/flashcards/cardio-pulmonary-bypass-800356/packs/1407355

In addition, ancrod promotes an indirect activation of the plasminogen-plasmin pathway. In the Stroke Treatment with Ancrod ... Intravenous ancrod for treatment of acute ischemic stroke: the STAT study-a randomized controlled trial. Stroke Treatment with ... Ancrod (Viprinex; Neurobiological Technologies, Emeryville, Calif) is the purified fraction of the Malayan pit viper venom. It ... but a trend toward more sICH with ancrod (5.2% versus 2%; P = .06).30 The ASP-II trial is currently enrolling patients with an ...

http://www.ajnr.org/content/30/4/649

http://www.ajnr.org/content/30/4/649?ijkey=78cd14270e410ac99e61fb5941fbfd00c53f33df&keytype2=tf_ipsecsha

... the German company that had discovered and started developing ancrod, and had acquired the rights to ancrod in 2002, after ... Ancrod became NTIs lead product; in 2006 Frieman estimated annual sales $500 million to $1 billion. The company collapsed when ... In 2004 NTI acquired Empire Pharmaceuticals, which had one product: ancrod (Viprinex). Empire had been formed by former ... the company was dissolved in 2009 after the failure of its drug candidate ancrod in a Phase III trial for ischemic stroke. The ...

https://en.wikipedia.org/wiki/Neurobiological_Technologies

Ancrod. For the treatment of established deep vein thrombosis; central retinal and branch vein thrombosis; priapism; pulmonary ...

https://www.drugbank.ca/categories/DBCAT000011

Ancrod. Estriol may decrease the anticoagulant activities of Ancrod.. Investigational. Androstenedione. The serum concentration ...

https://www.drugbank.ca/drugs/DB04573

Ancrod, the coagulating enzyme from Malayan pit viper (Agkistrodon rhodostoma) venom.. Nolan C, Hall LS, Barlow GH. ...

https://www.ncbi.nlm.nih.gov/pubmed?cmd=search&term=Hall+LS%5Bau%5D&dispmax=50

1991) Rapid anticoagulation using Ancrod for heparin-induced thrombocytopenia. Blood 78:2194-97PubMedGoogle Scholar ... 1989) Ancrod anticoagulation for cardiopulmonary bypass in heparin-induced thrombocytopenia and thrombosis. Ann Thor Surg 48: ...

https://link.springer.com/chapter/10.1007/978-3-642-51190-5_12

Ancrod - Batroxobin. Other. Acrosin - Prolyl endopeptidase - Pronase - Proprotein convertases (1, 2) - Subtilisin/Furin - ...

https://www.bionity.com/en/encyclopedia/Serine_protease.html

Ancrod - Batroxobin. Other. Acrosin - Prolyl endopeptidase - Pronase - Proprotein convertases (1, 2) - Subtilisin/Furin - ...

https://www.bionity.com/en/encyclopedia/Pancreatic_elastase.html

ANCROD (EC 3.4.21.74), BSA, goat and rabbit serum, and SLIGRL (PAR-2 Ag) were from Sigma-Aldrich. TFLLR (PAR-1 Ag), GYPGKF (PAR ... 3.83 ± 0.31 d for WT plus ANCROD; n = 6; P = 0.004) and at rejection had fewer infiltrating NK cells and MΦs (Fig. 1, b and c ... WT plus ANCROD), rejection was accompanied by significant NK cell and MΦ infiltration (Fig. 1 c). Both antAgs together had no ... 4, b-e). No mice received ANCROD in these experiments. Therefore, PAR-1 is required to generate MCP-1, MCP-3, and MCP-5 for ...

http://jem.rupress.org/content/205/8/1739.full

The primary purpose of this study is to determine whether a brief intravenous infusion of ancrod started within 6 hours of stroke onset improves functional outcome at 3 months. (strokecenter.org)
Description: Intravenous ancrod infused at a rate of 0.167 IU/kg/hr (0.6 mL/kg/hr) for 2 or 3 hours depending on the pretreatment fibrinogen level. (strokecenter.org)
How effective and safe is intravenous ancrod in the treatment of acute ischemic stroke? (essentialevidenceplus.com)
Hennerici MG, Kay R, Bogousslavsky J, Lenzi GL, Verstraete M, Orgogozo JM, ESTAT Investigators (2006) Intravenous ancrod for acute ischaemic stroke in the European Stroke Treatment with Ancrod Trial: a randomised controlled trial. (springermedizin.de)

Thrombocytopenia as side effect has never been noticed with ancrod in contrast to heparin. (wikipedia.org)
There are some patients for whom heparin is unsuitable and ancrod (a defibrinogenating enzyme) has been used as an alternative. (unboundmedicine.com)
We present a patient with heparin-induced thrombocytopenia in whom treatment ancrod was ineffective. (unboundmedicine.com)
Perioperative administration of ancrod showed no greater benefit when compared to unfractionated heparin. (cochrane.org)
Cines DB, Tomaski A, Tannenbaum S (1987) Immune en-dothelial-cell injury in heparin-associated thrombocytopenia. (springer.com)
Alternative pharmacologic means of anticoagulation include the use of low molecular weight heparin (LMWH), ancrod, warfarin, platelet inhibitors such as aspirin and dextran, as well as the thrombin inhibitors, hirudin or argatroban. (asahq.org)

Ancrod (current brand name: Viprinex) is a defibrinogenating agent derived from the venom of the Malayan pit viper. (wikipedia.org)
In 2004 NTI acquired Empire Pharmaceuticals, which had one product: ancrod (Viprinex). (wikipedia.org)

In clinical trials for ischemic stroke, ancrod increased the risk of intracebrral hemorrhage. (wikipedia.org)
Controlled trial of ancrod in ischemic stroke. (strokecenter.org)
Patients receive a one-time, 2-3 hour infusion of ancrod or placebo within six hours of the initial symptom onset of their ischemic stroke, and are then followed for three months to collect information on their functional status. (strokecenter.org)
the company was dissolved in 2009 after the failure of its drug candidate ancrod in a Phase III trial for ischemic stroke. (wikipedia.org)
In the article "Ancrod in Acute Ischemic Stroke: Results of 500 Subjects Beginning Treatment Within 6 Hours of Stroke Onset in the Ancrod Stroke Program", by Levy et al, 1 an author is missing from the byline. (ahajournals.org)
The Ancrod Stroke Study Investigators (1994) Ancrod for the treatment of acute ischemic brain infarction. (springermedizin.de)
The drug, also known by the generic name ancrod, is designed to help people who suffer an acute ischemic stroke, the most common type. (mylot.com)

Although other agents including platelet inhibitors (aspirin), anticoagulants (ancrod, heparins), and prourokinase have been used in the management of acute stroke, there is only poor or no evidence that these approaches improve outcome [ 4 , 9 , 10 ]. (hindawi.com)

One of the cleavage fibrinogen products, termed 'desAA-Fibrin', acts as cofactor for the tPA-induced plasminogen activation and an increased fibrinolysis results in return (profibrinolytic activity of ancrod). (wikipedia.org)
In rabbits with nephrotoxic nephritis, defibrination with ancrod provided protection when administered during the autologous phase, after extensive glomerular fibrin deposition had occurred and crescents and renal failure were developing. (nih.gov)
As previously reported, pre-transplant fibrinogen levels were depleted to 5% of the levels seen in control rats, and hearts rejected by ANCROD-treated rats contained no evidence of fibrin deposition ( 5 ). (rupress.org)

The blood viscosity in patients receiving ancrod is progressively reduced by 30 to 40% of the pretreatment levels. (wikipedia.org)
Ancrod decreases the blood viscosity in affected arteries, leads to less intense pain, improves physical limb mobility, and facilitates physical and ergo therapy. (wikipedia.org)

Yet the anti-clotting drug alternatives, including aspirin, the experimental iloprost and ancrod, can cause allergies and side effects as well. (mcall.com)

The rheological changes are readily maintained and the viscosity approaches pretreatment values very slowly (within about 10 days) after stopping ancrod. (wikipedia.org)
Whereas the first two types of treatment often give unsatisfactory results, a new rheological therapy using Ancrod seems to be successful. (cdc.gov)

Ancrod a similar enzyme from Agkistrodonrhodostoma can also be used to replace thrombin in the thrombin clotting time test. (slideserve.com)

As of 2017 ancrod was not marketed for any medical use. (wikipedia.org)

No fibrinopeptide A was cleaved off from the isolated abnormal molecule by thrombin or snake venoms (Reptilase and Ancrod) as evidenced by radioimmunoassay, high performance liquid chromatography and determination of the NH2-terminal amino acids. (biomedsearch.com)

The purpose of this study is to determine whether ancrod is effective and safe in the treatment of sudden sensorineural hearing loss (SSHL). (clinicaltrials.gov)

Inhibiting thrombosis by depleting fibrinogen from the recipients (using a snake venom protein, ANCROD) failed to achieve the same degree of survival, and under these conditions, infiltrating NK cells and macrophages (MΦs), rather than T cells, were observed in rejected grafts ( 6 ). (rupress.org)

Data from one of those trials, published in the Journal of the American Medical Association in May of 2000, found that patients who received the drug - called ancrod - intravenously over a 72-hour period had regained more function after three months than patients who got a placebo. (sunjournal.com)
While ancrod caused a slightly higher rate of bleeding in the brain - 5.2 percent compared with 2 percent for the placebo group - it did not cause an increase in deaths. (sunjournal.com)

and ancrod, a serine protease inhibitor that reduces fibrinogen levels. (aafp.org)

I.M.-Injection : Ancrod should not be injected i.m., because of rapid induction of neutralizing antibodies and thus drug resistance. (wikipedia.org)
appearance of neutralizing antibodies to ancrod with partial or total loss of ancrod activity (drug resistance). (wikipedia.org)
The half-life of ancrod is 3 to 5 hours and the drug is cleared from blood plasma, mainly renally. (wikipedia.org)
A major trail is being done on ancrod, a drug derived from the venom of the Malayan pit viper. (amazonaws.com)

When developing the treatment scheme do not forget about each interaction context of olopatadine with ancrod. (rosesturn.com)

As a more direct test, hypo-fibrinogenemic mice were generated with repeated ancrod injection. (biomedcentral.com)

Patients were treated with either low-molecular weight dextran and mannitol alone (group A) or in combination with ancrod (group B). (strokecenter.org)

Hearts from MCP-1 KO mice were transplanted into ANCROD-treated rats. (rupress.org)

In six patients suffering from severe secondary Raynaud's disease, Ancrod was injected subcutaneously for a 2 to 4 week period at a dose of 1 unit per kilogram of body weight per day. (cdc.gov)

The company collapsed when a Phase III trial of ancrod was halted early in December 2008 when an independent review committee looked at the interim data and found no signal of benefit. (wikipedia.org)
Plasma epirizole and postdexamethasone cortisol concentrations were determined by hplc up trial to 71 hours, ancrod and hydroxyitraconazole up transactions to 23 hours. (coconutoilbenefits.biz)

One of the first, an anticoagulant called Arvin, gained favor in the late 1960s after a doctor discovered that ancrod, a protein found in the venom of the Malayan pit viper, could treat blood clots in the legs. (news-medical.net)

We discuss the reasons for this and suggest that the combination of ancrod and danaparoid sodium is a logical one in such cases. (unboundmedicine.com)

ancrod' can also refer to. (oup.com)

Posted on June 18, 2018 Author Aubrey Comments Off on What are examples of Ancrod wrinkle fillers? (amberchildsafety.com)

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Development of an ischemic stroke survival score. (1/41)

Analysis of fibrin formation and proteolysis during intravenous administration of ancrod. (2/41)

The effect of angrod on the delayed hypersensitivity response in rats. (3/41)

A quantitative evaluation of anticoagulants in experimental nephrotoxic nephritis. (4/41)

The effects of defibrination with ancrod in experimental allergic glomerular injury. (5/41)

Fibrinogen depletion attenuates Staphyloccocus aureus infection by preventing density-dependent virulence gene up-regulation. (6/41)

Embolization itself stimulates thrombus propagation in pulmonary embolism. (7/41)

Soluble fibrin is the main mediator of Staphylococcus aureus adhesion to platelets. (8/41)

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Hyperlipidemias

Hydroxymethylglutaryl-CoA Reductase Inhibitors

Head and Neck Neoplasms

Risk Factors

Hearing Loss, Sudden

Hearing Loss, Sensorineural

Hearing Loss, Unilateral

Audiometry, Pure-Tone

Tympanic Membrane

Development of an ischemic stroke survival score. (1/41)

Analysis of fibrin formation and proteolysis during intravenous administration of ancrod. (2/41)

The effect of angrod on the delayed hypersensitivity response in rats. (3/41)

A quantitative evaluation of anticoagulants in experimental nephrotoxic nephritis. (4/41)

The effects of defibrination with ancrod in experimental allergic glomerular injury. (5/41)

Fibrinogen depletion attenuates Staphyloccocus aureus infection by preventing density-dependent virulence gene up-regulation. (6/41)

Embolization itself stimulates thrombus propagation in pulmonary embolism. (7/41)

Soluble fibrin is the main mediator of Staphylococcus aureus adhesion to platelets. (8/41)

Ancrod snake venom peptide

Double-blind, Randomized, Placebo-controlled Study on Efficacy, Safety and Tolerability of Ancrod in Patients With Sudden...

OBSERVATIONS ON EARLY DETECTION AND THERAPY OF THE DEFIBRINATION SYNDROME IN MENINGOCOCCEMIA,

Correction | Stroke

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Thrombin-like enzyme cerastobin elisa and antibody

Thrombin-like enzyme gloshedobin elisa and antibody

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