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Hematotoxicity In Vitro and Ex Vivo Compound Profiling

The main target organs for compound toxicity leading to either drug withdrawal or arrest of compound development as estimated in various studies [3], are classically pointing at liver, the cardiovascular system and bone marrow (hematotoxicity). Cardiovascular and hepatotoxicity were discussed in previous chapters and this chapter focuses on hematotoxicity. [Pg.415]

Hematotoxicity, defined as drug-induced altered production of peripheral blood cells, is most commonly associated with antiproliferative oncology compounds but is also caused by drugs for various indications, covering a wide pharmacology and chemical structure diversity (Table 17.1). This vast variety of chemical structures makes it difficult to predict hematotoxicity by in silica approaches and to model [Pg.415]

Hit and Lead Projiling. Edited by Bernard Faller and Laszlo Urban Copyright 2009 WILEY-VCH Verlag GmbH Co. KGaA, Weinheim ISBN 978-3-527-32331-9 [Pg.415]

Analgesic and Acetylsahcylic acid, aminopyrine, benoxaprofen, dipyrone, bucilla- [Pg.416]

Anticonvulsant Carbamazepine, ethosuximide, lamotrigine, mesantoin, phenytoin, trimefhadione, valproic acid [Pg.416]


See other pages where Hematotoxicity In Vitro and Ex Vivo Compound Profiling is mentioned: [Pg.415]    [Pg.416]    [Pg.420]    [Pg.426]    [Pg.430]    [Pg.436]    [Pg.415]    [Pg.416]    [Pg.420]    [Pg.426]    [Pg.430]    [Pg.436]   


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Compound profile

Compound profiling

Ex vivo

Ex vivo compound profiling

Hematotoxic

Hematotoxicity

In profiling

In vivo profiling

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