Relevant bibliographies by topics / Defibrotide

Academic literature on the topic 'Defibrotide'

Author: Grafiati
Published: 10 December 2022
Last updated: 28 January 2023

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Journal articles on the topic "Defibrotide"

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Richardson, Paul G., Marta Palomo, Nancy A. Kernan, Gerhard C. Hildebrandt, Nelson Chao, and Enric Carreras. "The importance of endothelial protection: the emerging role of defibrotide in reversing endothelial injury and its sequelae." Bone Marrow Transplantation 56, no. 12 (September 28, 2021): 2889–96. http://dx.doi.org/10.1038/s41409-021-01383-x.

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AbstractHepatic veno-occlusive disease/sinusoidal obstruction syndrome (VOD/SOS), a potentially life-threatening complication of hematopoietic cell transplantation (HCT), results from prolonged sinusoidal endothelial cell activation and profound endothelial cell damage, with sequelae. Defibrotide, the only drug approved in the United States and Europe for treating VOD/SOS post-HCT, has European Commission orphan drug designation for preventing graft-versus-host disease (GvHD), associated with endothelial dysfunction. This endothelial cell protector and stabilizing agent restores thrombo-fibrinolytic balance and preserves endothelial homeostasis through antithrombotic, fibrinolytic, anti-inflammatory, anti-oxidative, and anti-adhesive activity. Defibrotide also preserves endothelial cell structure by inhibiting heparanase activity. Evidence suggests that downregulating p38 mitogen-activated protein kinase (MAPK) and histone deacetylases (HDACs) is key to defibrotide’s endothelial protective effects; phosphatidylinositol 3-kinase/Akt (PI3K/AKT) potentially links defibrotide interaction with the endothelial cell membrane and downstream effects. Despite defibrotide’s being most extensively studied in VOD/SOS, emerging preclinical and clinical data support defibrotide for treating or preventing other conditions driven by endothelial cell activation, dysfunction, and/or damage, such as GvHD, transplant-associated thrombotic microangiopathy, or chimeric antigen receptor T-cell (CAR-T) therapy-associated neurotoxicity, underpinned by cytokine release syndrome and endotheliitis. Further preclinical and clinical studies will explore defibrotide’s potential utility in a broader range of disorders resulting from endothelial cell activation and dysfunction.
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&NA;. "Defibrotide." Reactions Weekly &NA;, no. 538 (February 1995): 7. http://dx.doi.org/10.2165/00128415-199505380-00024.

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Palmer, Katharine J., and Karen L. Goa. "Defibrotide." Drugs 45, no. 2 (February 1993): 259–94. http://dx.doi.org/10.2165/00003495-199345020-00007.

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&NA;. "Defibrotide." Reactions Weekly &NA;, no. 1113 (August 2006): 9. http://dx.doi.org/10.2165/00128415-200611130-00028.

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Coccheri, Sergio, and Giovanna Biagi. "Defibrotide." Cardiovascular Drug Reviews 9, no. 2 (June 1991): 172–96. http://dx.doi.org/10.1111/j.1527-3466.1991.tb00410.x.

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Moore, Julie M., and John W. Avery. "Defibrotide." Arteriosclerosis, Thrombosis, and Vascular Biology 32, no. 3 (March 2012): 541–44. http://dx.doi.org/10.1161/atvbaha.111.242776.

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Baker, Danial E., and Kendra Demaris. "Defibrotide." Hospital Pharmacy 51, no. 10 (October 2016): 847–54. http://dx.doi.org/10.1310/hpj5110-847.

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Tappe, William, Saurabh Aggarwal, Ozlem Topaloglu, and Massimo Iacobelli. "A Meta-Analysis Evaluating the Incidence of Bleeding Events With Intravenous Defibrotide Treatment Outside the Veno-Occlusive Disease/Sinusoidal Obstruction Syndrome Setting." Clinical and Applied Thrombosis/Hemostasis 26 (January 1, 2020): 107602962093520. http://dx.doi.org/10.1177/1076029620935202.

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Defibrotide is approved to treat hepatic veno-occlusive disease/sinusoidal obstruction syndrome (VOD/SOS) with renal/pulmonary dysfunction following hematopoietic cell transplantation (HCT) in adult and pediatric patients in the United States, and to treat severe hepatic VOD/SOS post-HCT in adult and pediatric patients aged >1 month in the European Union. The defibrotide prescribing information warns that defibrotide may increase bleeding risk in VOD/SOS patients. To broaden our understanding of the incidence of bleeding with defibrotide, we performed a meta-analysis of the published literature of defibrotide use outside of the post-HCT VOD/SOS setting. Of 1857 records identified, 125 reported on defibrotide; 23 contained data on bleeding events. The estimated overall incidence of bleeding events was 1% (95% confidence interval [CI]: 0%-2%) and 8% (95% CI: 3%-14%) in studies using intravenous defibrotide and studies with controls, respectively. The risk ratio for bleeding events with intravenous defibrotide versus controls was 0.36 (95% CI: 0.24-0.52; P < .00001) among studies with data on intravenous defibrotide and controls. This meta-analysis of defibrotide use outside of the post-HCT VOD/SOS setting suggests that the incidence of bleeding with defibrotide is lower than controls.
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Fareed, Jawed, Debra A. Hoppensteadt, Massimo Iacobelli, and Jeanine M. Walenga. "Defibrotide Does Not Cross-React with HIT Antibodies. Implications in the Management of HIT." Blood 108, no. 11 (November 16, 2006): 1054. http://dx.doi.org/10.1182/blood.v108.11.1054.1054.

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Abstract Defibrotide is a mammalian DNA derived antithrombotic and anti-ischemic agent that does not produce systemic anticoagulation. Heparin-induced thrombocytopenia (HIT) is an immune disease related to heparin exposure, in which patients are at risk of developing life- and limb-threatening thrombosis. Studies were performed to determine whether defibrotide cross-reacts with HIT antibodies. Sera from 141 clinically confirmed HIT patients were tested for platelet activation in the presence of defibrotide (1 – 100 μg/ml) and unfractionated heparin (1 – 100 μg/ml). 103 sera (73%) produced platelet aggregation and serotonin release activities with heparin. Only 4 samples (2%) showed a weak reactivity with defibrotide which was eliminated by heparinase treatment indicating heparin contamination in the patient sample. Further studies revealed that defibrotide does not complex with platelet factor 4 (PF4), and that prolonged incubation of defibrotide with platelet rich plasma does not mobilize PF4. Studies of patients treated with extended dosing of intravenous or oral defibrotide (n=270) demonstrated that HIT antibodies are not generated with defibrotide treatment. Studies carried out on the effect of purified IgG from HIT patients revealed that defibrotide blunts platelet activation and microparticle formation as measured by flow cytometry. These studies suggest that defibrotide may be a useful antithrombotic agent for the management of patients with HIT. Moreover, unlike heparin, defibrotide does not promote platelet activation, rather it is capable of suppressing the hypercoagulable state associated with HIT. Defibrotide is orally bioavailable and can be used for extended anticoagulant management of HIT patients.
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Park, Meerim, Hyeon Jin Park, Hyeon-Seok Eom, Jeong A. Park, Yeon Jung Lim, Jong Hyung Yoon, Hye Won Lee, Tak Yun, and Byung-Kiu Park. "Effects of Prophylactic Defibrotide for Veno-Occlusive Disease in Hematopoietic Stem Cell Transplantation." Blood 118, no. 21 (November 18, 2011): 4517. http://dx.doi.org/10.1182/blood.v118.21.4517.4517.

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Abstract Abstract 4517 Background: Defibrotide has recently been successfully used to treat veno-occlusive disease (VOD). We report the use of intravenous defibrotide for VOD prophylaxis in 49 patients who received hematopoietic stem cell transplantation (HSCT). This group was compared with a control group of 49 patients who underwent HSCT without defibrotide prophylaxis. Patients and methods: Data were collected retrospectively on 98 patients undergoing HSCT at the National Cancer Center, Goyang, Korea, between August 2005 and July 2008. During this period, defibrotide was randomly supplied to 49 patients free of charge by the compassionate use program. For 49 patients, VOD prophylaxis with 200 to 400 mg of defibrotide (25 mg/kg/day in children weighing less than 30 kg) administered intravenously 3 or 4 times daily was initiated from the start of conditioning and continued until 28 days post-HSCT. Results: VOD was diagnosed in 5 of 98 total patients (5.1%) at a median of 11 days post-HSCT (range: 10–14 days). VOD was graded as mild in 2 patients, moderate in 1, and severe in 2. The incidences of engraftment syndrome, thrombotic microangiopathy and VOD were not significantly different between the defibrotide group and the control group, although absolute incidences of each syndrome were lower in the defibrotide group. Patients who received prophylactic defibrotide showed earlier platelet engraftment (p<0.01) and lower activated prothrombin time (p=0.02) after HSCT. There was no day 100 treatment-related mortality (TRM) in the defibrotide group. Day 100 TRM occurred in two patients who did not receive defibrotide for VOD prophylaxis during allogeneic HSCT. Each patient was diagnosed with mild or severe VOD, and the direct causes of death were infection or VOD. Of the patients who were diagnosed with VOD, the overall survival at 100 days post HSCT was significantly higher in the defibrotide group compared to the control group (100% vs. 33.3 ± 27.2%, p<0.01). Defibrotide was well tolerated and was not discontinued in any patients. There was no grade 3 or 4 toxicity related to defibrotide or any worsening of clinical bleeding. Conclusions: Our data showed that the use of prophylactic defibrotide is safe and may have beneficial effects of defibrotide on hepatic endothelial damage following HSCT, with no TRM in defibrotide group. Considering there is no consensus on when to start treatment if a patient shows clinical features suggesting VOD, it could be important to use prophylactic defibrotide in advance for improved VOD outcomes. Disclosures: No relevant conflicts of interest to declare.
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Dissertations / Theses on the topic "Defibrotide"

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Stanescu, Ioana [Verfasser], and Bruno [Akademischer Betreuer] Reichart. "Der Einfluss von Defibrotide auf die Herzfunktion und den myokardialen Schaden in einem ex vivo Perfusionsmodell der kardialen Xenotransplantation / Ioana Stanescu. Betreuer: Bruno Reichart." München : Universitätsbibliothek der Ludwig-Maximilians-Universität, 2016. http://d-nb.info/1105373932/34.

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Hamelmann, Hannah [Verfasser]. "Einfluss von Anti-Thymozyten-Globulin und Defibrotid auf die Proliferation, Migration und angiogene Aktivität von Endothelzellen / Hannah Lena Hamelmann." Berlin : Medizinische Fakultät Charité - Universitätsmedizin Berlin, 2020. http://d-nb.info/1212435303/34.

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Hamelmann, Hannah Lena [Verfasser]. "Einfluss von Anti-Thymozyten-Globulin und Defibrotid auf die Proliferation, Migration und angiogene Aktivität von Endothelzellen / Hannah Lena Hamelmann." Berlin : Medizinische Fakultät Charité - Universitätsmedizin Berlin, 2020. http://d-nb.info/1212435303/34.

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Books on the topic "Defibrotide"

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Ulutin, O. N. International Congress on Thrombosis, 8th, Istanbul, June 1984, Defibrotide Symposium (Haemostasis,). S. Karger AG (Switzerland), 1986.

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Book chapters on the topic "Defibrotide"

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Frasca’, G. M., B. Stagni, C. Raimondi, A. Vangelista, and V. Bonomini. "Clinical Experience with an Antithrombotic Agent (Defibrotide) in Glomerular Diseases. Preliminary Results." In Current Therapy in Nephrology, 25–27. Boston, MA: Springer US, 1989. http://dx.doi.org/10.1007/978-1-4613-0865-2_5.

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Ulutin, O. N., S. Balkuv-Ulutin, M. S. Ugur, T. Ulutin, Y. Özsoy, and G. Çizmeci. "The Pharmacology and Clinical Pharmacology of Defibrotide: A New Profibrinolytic, Antithrombotic and Anti-Platelet Substance." In Advances in Experimental Medicine and Biology, 429–38. Boston, MA: Springer US, 1990. http://dx.doi.org/10.1007/978-1-4615-3806-6_46.

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Pellegatta, F., E. Ferrero, A. Marni, S. Chierchia, D. Forti, and M. E. Ferrero. "The anti-ischemic drugs defibrotide and oligotide analogously inhibit leukocyte-endothelial cell adhesion in vitro." In Transplant International, 420–24. Berlin, Heidelberg: Springer Berlin Heidelberg, 1996. http://dx.doi.org/10.1007/978-3-662-00818-8_101.

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Schrör, K., Ch Thiemermann, and P. Löbel. "Stimulation of Vascular Prostacyclin Formation by Defibrotide: A New Strategy for Treatment of Acute Myocardial Ischaemia." In Limitation of Infarct Size, 83–93. Berlin, Heidelberg: Springer Berlin Heidelberg, 1989. http://dx.doi.org/10.1007/978-3-642-73585-1_12.

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Pescador, R., R. Tettamanti, L. Salvetti, A. Conto, R. Porta, M. Mantovani, and L. Ferro. "Defibrotide’s Activity on Leukocytes and Platelets in Rabbits with Diet-Induced Atherosclerosis." In Mediators in the Cardiovascular System: Regional Ischemia, 323–27. Basel: Birkhäuser Basel, 1995. http://dx.doi.org/10.1007/978-3-0348-7346-8_44.

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"Defibrotide." In Meyler's Side Effects of Drugs: The International Encyclopedia of Adverse Drug Reactions and Interactions, 1071. Elsevier, 2006. http://dx.doi.org/10.1016/b0-44-451005-2/00384-3.

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"Defibrotide." In Meyler's Side Effects of Drugs, 861. Elsevier, 2016. http://dx.doi.org/10.1016/b978-0-444-53717-1.00590-4.

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"Defibrotide Sodium." In ASHP® Injectable Drug Information™, 458–60. ASHP, 2021. http://dx.doi.org/10.37573/9781585286850.115.

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Conference papers on the topic "Defibrotide"

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Porta, R., R. Pescador, R. Niada, M. Mentavani, and G. Prino. "PROFIBRINOLYTIC ACTIVITY OF DEFIBROTIDE IS PTOSTACYCLIN-INDEFENDEMT." In XIth International Congress on Thrombosis and Haemostasis. Schattauer GmbH, 1987. http://dx.doi.org/10.1055/s-0038-1643151.

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The profibrinolytic, antithrombotic and thrombolytic activities of Defibrotide, a polydeoxyribonucleotide obtained from mammalian lungs, have been previously described. Defibrotide is also able to promote the generation and release into the circulation of prostacyclin and of plasminogen activator factor (tPA) from vascular walls. These two last activities, i.e., PGI2 and tPA stimulation, could be of importance in the profibrinolytic activity of Defibrotide. In an attempt to clarify the profibrinolytic mechanism/s of Defibrotide, the role of PGI2 generation in this activity was investigated in rabbits in which the cycloxygenase pathway was blocked with Indcmethacin. Male rabbits were treated with Indcmethacin, 10 ng/Kg, i.v., 20 minutes or 2 hours before Defibrotide administration. Defibrotide was injected i.v. into rabbits at two dose levels (16 or 64 rrg/Kg). Rabbits treated with Defibrotide only were used as controls. The profibrinolytic activity was evaluated measuring the lysed area of normal human fibrin plates induced by euglobulin fraction obtained from plasma. Results are reported in the Table.Indomethacin (Indo) administered 20 min (*) or 2h (**) before Defibrotide.AN3VA: N.S. vs. Vehicle + D 12.5 or D 50 ng/Kg i.v.; P< 0.01 vs. basal.The results reported here demonstrate that the profibrinolytic activity of Defibrotide is independent of PGI2 generation: Indcmethacin pro treatment was unable to suppress or to reduce the fibrinolytic response of the rabbit to Defibrotide.
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Kindel, G., J. Fareed, and U. Cornelli. "EFFECTS OF DEFIBROTIDE TREATMENT ON THE PLASMA AND SERUM INDUCED CONTRACTION OF RABBIT AORTIC STRIP IN RELATION TO THE PATHOPHYSIOLOGY OF MYOCARDIAL INFARCTION." In XIth International Congress on Thrombosis and Haemostasis. Schattauer GmbH, 1987. http://dx.doi.org/10.1055/s-0038-1643147.

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Several clinical and experimental studies have demonstrated the efficacy of a polydeoxyribonucleotide (Defibrotide) in myocardial ischemic disorders and peripheral arterial diseases. In attempts to investigate the mechanisms of action of this agent, we used a modified rabbit model of hemodynamics and an isolated rabbit aortic strip preparation. Intravenous bolus administration of Defibrotide at 5-50 mg/kg did not produce any changes in the mean arterial blood pressure up to 3 hours. Defibrotide treated rabbits also resisted human serum-stasis and stasis alone induced venous and arterial thrombus formation. Serum and plasma from Defibrotide treated animals were tested for their direct contractile and procontractile (synergistic with an epinephrine stimulus) activities on rabbit aortic strips. In contrast to plasma and serum from saline treated rabbits, both serum and plasma produced relatively weak or no effects. The dose-contrac-tion responses were shifted to the right suggesting that serum from Defibrotide treated animals contained much lesser amounts of contractile substances. This data indicates blood from Defibrotide treated rabbits is compositionally different than normal, either due to lack of cellular product formation (thromboxane B 2, serotonin) or due to the generation of endothelial products which are inhibitory to the contractile effects of substances generated during the formation of a thrombus. Plasma thromboxane B2/6 keto-PGFia ratios were also found to be much higher in Defibrotide treated groups when compared to the saline groups. The observed therapeutic effect of Defibrotide in acute myocardial infarction may be linked with the inhibition of the formation of thrombus and with the mediation of vascular spasm due to the generation of inhibitory substances or the lack of generation of spasmogenic substances.
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NIADA, R., R. Porta, R. Tettamanti, R. Pescador, M. Mantovani, and G. Prino. "DEFIBROTIDE IN EXPERIMENTAL MYOCARDIAL ISCHEMIA IN THE CAT: EFFECTS ON HEMODYNAMICS, ENERGY METABOLISM AND INFARCT SIZE." In XIth International Congress on Thrombosis and Haemostasis. Schattauer GmbH, 1987. http://dx.doi.org/10.1055/s-0038-1643152.

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Defibrotide was able to prevent the hemodynamic and biochemical alterations caused by acute myocardial ischemia (AMI) induced by coronary occlusion in the cat when infused 3.5 h before and 5 h after left anterior descending coronary artery (LAD) occlusion. In the platelet perfused heart, Defibrotide was a selective stimulator of coronary vascular PGI^ but not of platelet thromboxane formation. The present study was designed both to investigate the effects of Defibrotide injected 30 min after the induction of acute myocardial ischemia (AMI) in the cat and to evaluate the ability of this drug to reduce infarct size. In the first set of experiments a permanent ligature (5 hours) was placed around LAD. ST segment from ECG, mean aortic pressure (MAP), heart rate (HR) and the pressure-heart rate index (PRI) were considered. Plasma and tissue creatine phosphckinase activity (CFK), tissue lactate and ATP were measured by enzymatic kits from Boehringer Biochemia. 30 min after coronary occlusion a loading dose of Defibrotide (32 ng Kg-1 ) was administered i.v. immediately followed by an infusion (32 ng Kg-1 h 4.5 h-1) MAP, HR and PRI were not modified either by AMI or by the infusion of Defibrotide. AMI-ST segment increases were reduced by Defibrotide from 0.5 h after the beginning of the treatment (—49% vs. AMI control) to the and of experiments (-83% vs. AMI control after 5 h occlusion period). Plasma CFK was reduced from 2.5 h after the beginning of the treatment (-29%) till the end of experiments (-52%). Ischemic tissue CFK, lactate and ATP were normalized by Defibrotide. In the second set of experiments the animals were infused with Defibrotide (50 or 200 mg Kg-1 h-1 , i.v.) starting 2 hours before coronary ligature. The infusion was maintained throughout the 5 h occlusion period. The risk and infarct areas were measured by Evans blu and nitroblue tetrazoliun staining. The 51 ± 3% of risk area was infarcted in AMI control cats. Defibrotide at the two tested doses significantly reduced these infarct areas to 42 ± 4% and 34 ± 2% of risk areas respectively. The beneficial effects of Defibrotide observed in AMI could be attributed both to its ability to enhance PGI2 release from vascular walls and to improved local tissue oxygenation and energy supplies. However it could be taken into account a direct cytoprotective action.
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Kumar, A., J. Fareed, W. H. Wehrmacher, D. Hoppensteadt, O. Ulutin, and J. M. Walenga. "ENDOTHELIAL FUNCTION MODULATION AND CONTROL OF VASCULAR AND THROMBOTIC DISORDERS: EXPERIMENTAL RESULTS WITH A POLYDEOXY RIBONUCLEOTIDE AGENT DEFIBROTIDE." In XIth International Congress on Thrombosis and Haemostasis. Schattauer GmbH, 1987. http://dx.doi.org/10.1055/s-0038-1643149.

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Numerous approaches with single and multiple drugs modulating protease cascade, platelet function and blood viscosity and to reduce blood lipids to manage thrombotic processes have been tried. Defibrotide, a polydeoxyribonucleotide, (Mr =17,000) offers a new approach to vascular and related thrombotic processes as it acts via modulation of endothelial cell function. We have used a primate model (Macaca mulatta) to study the endogenous action of this agent after the oral (10-25 mg/kg) and intravenous (5-10 mg/kg) administration. This agent produced no effect on clotting tests and ex vivo laboratory findings but rather it elevated the t-PA (antigen and functional), protein C (antigen and functional), prostacyclin and decreased thromboxane, 01.2-antiplasmin (functional) and t-PA inhibitor (functional) in both studies. These observations suggest that Defibrotide modulates endothelial function. Hepatic isolation in rabbits totally blocked the antithrombotic actions of Defibrotide suggesting that this agent is converted into an active product endogenously. Pretreatment of Defibrotide with nucleases also resulted in a complete loss of its actions. Defibrotide produced dose dependent antithrombotic actions in animal models (rabbit venous stasis and rat vena caval ligation) after either intravenous or oral administration. Blood pressure, heart rate, respiration and kidney function were not altered by it. No effect on bleeding time was noted in any studies. Upon oral administration this drug produced pharmacologic action after 2 hours whereas after intravenous administration, the action peaked at 30 minutes. Defibrotide exhibited cytoprotective effects towards endothelial lining of the vascular smooth muscles characterized by microscopic studies. In summary Defibrotide is an endothelial support agent whose multicomponent actions are primarily mediated via the physical and functional modulation of the endothelial cells in the vascular system.
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Pescador, R., R. Porta, R. Niada, M. Mantovani, and G. Prino. "DEFIBROTIDE DECREASES CHOLESTEROL CONTENT IN HYPERCHOLESTEROLEMIC RABBIT AORTA, WITH NO MODIFICATION OF PLASMA OR LIPOPROTEIN CHOLESTEROL." In XIth International Congress on Thrombosis and Haemostasis. Schattauer GmbH, 1987. http://dx.doi.org/10.1055/s-0038-1643153.

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Defibrotide was shown to stimulate the production of endogenous PGI2 from rat and hamster aortic tissue, as well as the production of PGi2 frcm the coronary vascular bed in the platelet perfused heart model. This effect was only seen in presence of platelets. Durirg the infusion period with Defibrotide thromboxane release remained unaffected while platelet cAMP rised. Defibrotide, was also able to reduce the secretion of ATP from platelets as well as to deaggregate platelet cluTps. It has been postulated that long-term administration of stable PGI^ metabolites or analogues could be a more useful means of enhancing cholesterol and cholesteryl ester mobilization out of the arterial “ foam” cell during early stages of cardiovascular disease. These observations prompted us to administer Defibrotide i.v. to cholesterol fed rabbits to verify if it could cause a decrease in cholesterol content of aortas. Aorta cholesterol was evaluated by gas chromatography. Plasma or lipoprotein lipids were assayed by enzymatic kits from Boehringer Biochemia. Plasma lipoproteins were separated by density gradient ultracentrifugation. Platelet aggregation was carried out with ADP using an optical aggregometer to find out the effective aggregatory concentration fifty (EC). Histology of the rabbit hearts was performed by optical microscopy on heart sections coloured with hematoxylin-eosine. Defibrotide caused a decrease (-49%, P < 0.05, vs. cholesterol fed rabbits treated with placebo) in cholesterol content of aortas with no modification of total plasma cholesterol, triglyceride and phospholipid. The cholesterol, triglyceride, phospholipid and protein of plasma lipoproteins were not affected too. The EC of rabbits treated with Defibrotide was 50 normalized (-9%, N.S. vs. control animals fed the normal diet and treated with placebo; cholesterol fed animals treated with placebo: -32%, P< 0.05 vs. control animals fed the normal diet). Vascular lesions in the hearts of animals treated with Defibrotide had a lower rate (33%) in comparison to that (87%) of animals fed with cholesterol and treated with placebo. It is concluded that the ability of Defibrotide to stimulate vascular PGI2 formation and to reduce platelet sensitivity could be helpful in reducing the amount of cholesterol in the cardiovascular system in atherosclerotic prone situations.
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Palmieri, G., R. Palmieri, G. Ambrosi, R. Ferraro, L. Bucci, and A. M. Agarthi. "DEFIBROTIDE VS. HEPARIN IN ACUTE THROMBOFLEBITIS THERAPY." In XIth International Congress on Thrombosis and Haemostasis. Schattauer GmbH, 1987. http://dx.doi.org/10.1055/s-0038-1643145.

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Defobrotide(D) a natural polydeoxyribonucleotide of mammalian lung origin is a new substance with no anticoagulant or hemodinamic effects?it has shown considerable profibrinolytic and antithrombotic activities. The ability of (D) to increase generation of prostaci-clmCPGI2) from vascular tissue has been demonstrated; this substance also promotes substantial release from vascular tissues of a plasminogen activator factor which plays an important role in preventing thrombotic oclusion of vascular segments.Widely accepted therapies in deep venous thrombosis and Acute Thromboflebitis (A.f.; are based on anticoagulant treatments (heparin and/or oral anticoagulant agentsWe have evaluated the efficacy of (D> in (A.T.) vs. heparin in 40 pts.(28 females 12 males;mean age=50) with an open randomized study.Group A:20 pts.have been administered CD; 200mg.four times a day l.m. for 10 days.Group B:20 pts.have been administered Sodic Heparin 30000 U.I. intravenously with successive dosage based upon APTT values.Both groups have been treated with an oral anti coagulant agentCacenocoumaro1) after the tenth day.No clinical differences between the treatments have been observed and in no pts. treated with CD; we noted significant changes m laboratory parameters evaluated: complete blood count,glycemia BUN creatinine ALT AST LDH.Clinical eficacy was excellent in both groups also supported by augmented fibrinolysis and instrumental improvement(strain-gauge plethismography;.The absolute safety of (D> therapy shows its possible alternative role when compared to heparin treatment in (A.T.> of any origin.
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Milazzotto, F., M. Carelli, C. Citone, G. Di Macro Tullio, G. C. Gambelli, P. Giampaolo, U. Malinconico, C. Polizzi, and U. Cornelli. "EFFECTIVENESS OF DEFIBROTIDE IN THE TREATMENT OF ACUTE MYOCARDIAL INFARCTION." In XIth International Congress on Thrombosis and Haemostasis. Schattauer GmbH, 1987. http://dx.doi.org/10.1055/s-0038-1643146.

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Defibrotide (D) is an extractive polydesoxyribonucleotide. In preclinical studies the product was shown to be active as a pro -fibrinolytic, antithrombotic and thrombolytic agent while comply tely devoid of anticoagulant activity. In animal models, D was found to afford striking protection from the effects of acute lethal and non lethal myocardial ischemia as well as from myo -cardial injury following reperfusion. In this open single - blim trial, D was administered to patients with acute myocardial infaj ction (AMI) for the prevention of complicating arrhythmias; throy bus formation, pericarditis, etc.Sixty patients with AMI were divided randomly into two groups of 30 patients each. One group was treated with D by 6-hour drip infusion for 3 consecutive days (2.8 g on the first day, then 2.4 g daily). The other group was treated with equal volumes of physiological salt solution. All patients received conventional trea_t ment for AMI. The two trial groups were sufficiently homogeneous in terms of AMI type, age and sex distribution, PCT, Forrester index, Holter, and Peel index. D treatment proved effective in reducing the incidence of severe arrhythmia (p < 0.05), thrombus formation (p < 0.05), and pericarditis (p < 0.01). CPK, TT and PTT readings were not modified by the treatment; the incidence of post-AMI angina and the number of deaths (4 in each group) were similar in the two groups. The results of this pilot study are encouraging; further clinical trials are currently in progress to assess D activity in larger groups of patients treated with the product at higher dosages.
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8

Ulutin, O. N., G. Cizmeci, U. Cornelli, and J. Fareed. "CLINICAL AND LABORATORY STUDIES ON THE EFFECTIVENESS OF DEFIBROTIDE IN PERIPHERAL VASCULAR DISEASE OF ATHEROSCLEROTIC ORIGIN." In XIth International Congress on Thrombosis and Haemostasis. Schattauer GmbH, 1987. http://dx.doi.org/10.1055/s-0038-1643148.

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Abstract:
Defibrotide is a derivative of polydeoxyribonucleotide extracted from bovine lung which has been found to produce profound activation of endothelial cells as evidenced by the increase of tissue plasminogen activator (t-PA) and prostacyclin levels in animal models. Administration of a 600 mg dose daily for six weeks to patients with peripheral obliterative diseases resulted in significant clinical improvements in post-treatment exercise tests and radionuclide arteriography. Results were consistent with improvements in the circulation. Ex vivo blood analysis showed marked increases in the production of t-PA and prostacyclin levels. Other laboratory tests were also suggestive of activated endothelial states. Platelet C-AMP levels were increased, whereas MDA and TXB2 levels were reduced. No systemic anticoagulation was observed in terms of alterations of the global coagulant tests (PT, APTT, etc.). These studies suggest that Defibrotide mainly acts via the modulation of the endothelial function and acts in a novel fashion in contrast to other drugs used in this area.
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9

Lobel, P., M. Palmer, and K. Schor. "CHRONIC ORAL DEFIBROTIDE STIMULATES VASCULAR PGI2 AND INHIBITS ATHEROSCLEROTIC PLAQUE FORMATION IN CHOLESTEROL-FED RABBITS." In XIth International Congress on Thrombosis and Haemostasis. Schattauer GmbH, 1987. http://dx.doi.org/10.1055/s-0038-1643150.

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Abstract:
Defibrotide (DEF) is a polydeoxyribonucleotide fraction from bovine lung, possessing profibrinolytic and PGI2 stimulating properties. Male rabbits were fed for 4 months a standard laboratory diet (150 g/day) without (A) or with (B) DEF or a cholesterol (1%) supplemented diet without (C) or with (D) DEF (60 mg/kg x day) was administered orally (drinking water) and withdrawn 24-36 h prior to the acute experiments.DEF did not change the elevated serum cholesterol: 18 ± 2 (C) vs. 26 ± 5 (D) mM but significantly reduced the plaque formation in the aorta from 4.5 ± 0.3 (C) to 3.3 ± 0.2 (D) (subjective score). Collagen induced (0.6 pg/ml) thromboxane formation and ATP release was significantly reduced by DEF: 55+2 (C) vs. 42 ± 2 (D) ng/ml TXB2; 152 ± 11 (C) vs. 74±5 (D) AU ATP (platelet rTch plasma). DEF significantly increased the basal and bradykinin (Bk, 30 nM) stimulated PGI2 release from rabbit aorta preparations in Krebs buffer, while the PGI2 forming capacity (arachidonic acid, AA, 30 pg/ml) was unchanged Furthermore, the iloprost (30 nM) stimulated cAMP was significantly elevated by DEF in both control: 115 ± 10 (A) vs. 155 ± 18 (B) pmoles/1 and cholesterol-fed rabbits: 120 ± 14 (C) vs. 172 ± 9 (D). DEF, directly added to the platelets in vitro did not inhibit platelet activation up to 100 pg/ml.The data demonstrate a 2-3-fold stimulation of basal and hormone (Bk) induced PGI2 formation of control and sclerotic rabbit aorta after 4 months DEF treatment while the atherosclerosis per se does not significantly change these parameters. DEF treatment also significantly reduces platelet hyperreactivity at unchanged serum ch() lesterol. Both properties might be useful to prevent complication’s of atherosclerosis, such as myocardial infarction and stroke.
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