Publications by authors named "A Naggi"

Article Synopsis
  • Heparanase is a key enzyme in the breakdown of heparan sulfate, contributing to tumor growth and metastasis, making it a target for cancer treatments.
  • Researchers synthesized specific trisaccharides and a tetrasaccharide that inhibit heparanase activity, focusing on glycol-split versions as potential inhibitors.
  • Studies using STD NMR and molecular docking revealed that these glycol-split trisaccharides had stronger binding and inhibitory effects against heparanase compared to their intact forms, providing insight into their mechanisms.
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Introduction: Heparins, naturally occurring glycosaminoglycans, are widely used for thrombosis prevention. Upon application as anticoagulants in cancer patients, heparins were found to possess additional antitumor activities. Ectonucleotidases have recently been proposed as novel targets for cancer immunotherapy.

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Several publications have recently proposed NMR spectroscopy to evaluate the critical quality attributes (CQA) of pentosan polysulfate sodium (PPS), the active ingredient of Elmiron™ approved to treat interstitial cystitis. PPS is a polymer of sulfated β(1-4)-d-xylopyranose residues randomly substituted by 4-O-methyl-glucopyranosyluronic acid, containing, beyond the main xylose-2,3-O-disulfate repetitive unit, some minor residues that can be marker of both the starting material and preparation process. In the present study we assigned some previously unknown cross-peaks in H-C HSQC NMR of PPS related to its minor sequences adding additional details to its CQA.

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Objective:  Danaparoid sodium is a biopolymeric complex drug composed of the most abundant heparan sulfate (HS) followed in descending order by dermatan sulfate (DS) and chondroitin sulfate (CS). This composite nature explains its peculiar antithrombotic and anticoagulant properties and make it particularly advantageous when the risk of heparin-induced thrombocytopenia occurs. A specific control of the danaparoid composition is required by the Ph.

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In renal transplantation, chronic transplant dysfunction (CTD) is associated with increased PCSK9 and dyslipidemia. PCSK9 is an enzyme that increases plasma cholesterol levels by downregulating LDLR expression. We recently showed increased PCSK9-syndecan-1 interaction in conditions of proteinuria and renal function loss.

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