Drafts by Sudipta Samadder
Evaluating the Potential of Heparin to Inhibit the Viral Entry of SARS-CoV-2, 2021
The well known anticoagulant agent, Heparin, is a member of the polyanionic polysaccharides
calle... more The well known anticoagulant agent, Heparin, is a member of the polyanionic polysaccharides
called glycosaminoglycans (GAGs). The molecule consists of alternating hexuronic acid and d-glucosamine residues joined by glycosidic linkages (Young, 2008). This gives heparin the appearance of a long, linear sulfated chain with the highest negative charge density of any known biomolecule (Hippensteel et al, 2020). The anticoagulant activity of heparin is attributed to a 3-O-sulfate and 6-O-sulfate containing pentasaccharide sequence or a minimum eight-repeating disaccharide units containing the pentasaccharide sequence which can establish binding sites that allow heparin to selectively and strongly interact with various proteins (Hao et al, 2019). The most well-characterized protein interaction is with the serine protease inhibitor called antithrombin-III (AT3), which gives heparin the ability to catalyze the inactivation of factor Xa or thrombin (Hippensteel et al, 2020). This simultaneously inhibits both thrombin generation and thrombin activity in the blood circulation, thus inhibiting blood coagulation. Since coagulation has been found to be particularly active early in the course of the novel Coronavirus Disease 2019 (COVID-19), anticoagulant therapy has proven to have the greatest impact before the disease advances to the hyperinflammatory state that can characterize the later stages of the disease (Antiviral Therapy, n.d). The high affinity interaction of heparin with a variety of proteases can characterize heparin with many other pharmacological properties such as anti-inflammatory, anti-viral, anti-angiogenesis, anti-neoplastic, and antimetastatic effects (Hao et al, 2019). Despite the mounting investigation of heparin’s effectiveness in treating the adverse side effects of COVID-19, there is still limited clinical data linking heparin therapy to meaningful antiviral outcomes. Hence, this paper evaluates the significant potential of heparin as an antiviral agent to inhibit the entry of the SARS-CoV-2 virus and thus revolutionize therapy for COVID-19.
Papers by Sudipta Samadder
Heparin is an anticoagulant medicine that prevents the formation of harmful blood clots in the ve... more Heparin is an anticoagulant medicine that prevents the formation of harmful blood clots in the vessels. Following the outbreak of the novel coronavirus disease 2019 (COVID-19), heparin has helped to improve the health of affected patients beyond its anticoagulant effects. The potential antiviral activity of heparin has attracted speculation due to its highly sulfated profile, which allows it to have a high binding affinity to a wide range of viral components. Heparin’s successful binding to the ZIKA virus, human immunodeficiency virus, as well as the SARS CoV and MERS CoV spike proteins have demonstrated its potential to inhibit the entry of SARS-CoV-2 into the body. A high degree of sequence homology also enables heparin to have inhibitory binding potential on viral components. The SARS-CoV-2 virus exhibits significant differences in its spike glycoprotein (SGP) sequence compared to other coronaviruses. The SGP sequence in SARS-CoV-2 contains additional potential glycosaminoglycan ...
Journal of Affective Disorders
Books: Non-fiction by Sudipta Samadder
Golden Meteorite Press, 2021
Decoding the Antikythera Mechanism: Mystery of the Ancient World provides a detailed look at The ... more Decoding the Antikythera Mechanism: Mystery of the Ancient World provides a detailed look at The Antikythera Mechanism, an Ancient Greek mechanical device described as the “oldest example of an analogue computer”. The chapters delve into the discovery of the Antikythera Mechanism, its mechanism of action, and its importance today. The book was written under the guidance of Dr. Austin Mardon, recipient of the Order of Canada.
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Drafts by Sudipta Samadder
called glycosaminoglycans (GAGs). The molecule consists of alternating hexuronic acid and d-glucosamine residues joined by glycosidic linkages (Young, 2008). This gives heparin the appearance of a long, linear sulfated chain with the highest negative charge density of any known biomolecule (Hippensteel et al, 2020). The anticoagulant activity of heparin is attributed to a 3-O-sulfate and 6-O-sulfate containing pentasaccharide sequence or a minimum eight-repeating disaccharide units containing the pentasaccharide sequence which can establish binding sites that allow heparin to selectively and strongly interact with various proteins (Hao et al, 2019). The most well-characterized protein interaction is with the serine protease inhibitor called antithrombin-III (AT3), which gives heparin the ability to catalyze the inactivation of factor Xa or thrombin (Hippensteel et al, 2020). This simultaneously inhibits both thrombin generation and thrombin activity in the blood circulation, thus inhibiting blood coagulation. Since coagulation has been found to be particularly active early in the course of the novel Coronavirus Disease 2019 (COVID-19), anticoagulant therapy has proven to have the greatest impact before the disease advances to the hyperinflammatory state that can characterize the later stages of the disease (Antiviral Therapy, n.d). The high affinity interaction of heparin with a variety of proteases can characterize heparin with many other pharmacological properties such as anti-inflammatory, anti-viral, anti-angiogenesis, anti-neoplastic, and antimetastatic effects (Hao et al, 2019). Despite the mounting investigation of heparin’s effectiveness in treating the adverse side effects of COVID-19, there is still limited clinical data linking heparin therapy to meaningful antiviral outcomes. Hence, this paper evaluates the significant potential of heparin as an antiviral agent to inhibit the entry of the SARS-CoV-2 virus and thus revolutionize therapy for COVID-19.
Papers by Sudipta Samadder
Books: Non-fiction by Sudipta Samadder
called glycosaminoglycans (GAGs). The molecule consists of alternating hexuronic acid and d-glucosamine residues joined by glycosidic linkages (Young, 2008). This gives heparin the appearance of a long, linear sulfated chain with the highest negative charge density of any known biomolecule (Hippensteel et al, 2020). The anticoagulant activity of heparin is attributed to a 3-O-sulfate and 6-O-sulfate containing pentasaccharide sequence or a minimum eight-repeating disaccharide units containing the pentasaccharide sequence which can establish binding sites that allow heparin to selectively and strongly interact with various proteins (Hao et al, 2019). The most well-characterized protein interaction is with the serine protease inhibitor called antithrombin-III (AT3), which gives heparin the ability to catalyze the inactivation of factor Xa or thrombin (Hippensteel et al, 2020). This simultaneously inhibits both thrombin generation and thrombin activity in the blood circulation, thus inhibiting blood coagulation. Since coagulation has been found to be particularly active early in the course of the novel Coronavirus Disease 2019 (COVID-19), anticoagulant therapy has proven to have the greatest impact before the disease advances to the hyperinflammatory state that can characterize the later stages of the disease (Antiviral Therapy, n.d). The high affinity interaction of heparin with a variety of proteases can characterize heparin with many other pharmacological properties such as anti-inflammatory, anti-viral, anti-angiogenesis, anti-neoplastic, and antimetastatic effects (Hao et al, 2019). Despite the mounting investigation of heparin’s effectiveness in treating the adverse side effects of COVID-19, there is still limited clinical data linking heparin therapy to meaningful antiviral outcomes. Hence, this paper evaluates the significant potential of heparin as an antiviral agent to inhibit the entry of the SARS-CoV-2 virus and thus revolutionize therapy for COVID-19.