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Central nervous system drug penetration

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    Skip to search form Skip to main content. Addressing central nervous system CNS penetration in drug discovery: basics and implications of the evolving new concept. Although there are multiple reasons, many failures are due to underestimating the complexity of the brain, also in terms of pharmacokinetics PK. View on PubMed. Alternate Sources.
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    Over the past decade, we have made considerable progress in establishing diffuse intrinsic pontine glioma DIPG as a disease entity and developing preclinical tools to interrogate potential therapeutics. However, translation to improved clinical outcomes in children with DIPG has not yet been realized. This is in part due to difficulties encountered in delivering active drugs adequately to the tumor site. However, most preclinical evaluations gloss over the fundamental concepts of central nervous system CNS pharmacokinetics and requirements needed to optimize drug delivery and exposure and translate this into efficacious therapy. This article discusses not only the blood:brain barriers but additional barriers to drug delivery for CNS tumors and pharmacokinetic principles that need to be addressed and considered. A critical determinant of drug efficacy is achieving adequate exposure of an active agent, in its unbound free state, at its site of action.
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    Despite enormous efforts, achieving a safe and efficacious concentration profile in the brain remains one of the big challenges in central nervous system CNS drug discovery and development. Although there are multiple reasons, many failures are due to underestimating the complexity of the brain, also in terms of pharmacokinetics PK. While increasing BBB permeability may shorten the onset of drug action, an increase in the total amount in brain may not necessarily increase the relevant drug concentration at the pharmacological target. Since the traditional Kp ratio is based on a crude homogenization of brain tissue, it ignores the compartmentalization of the brain and an increase favors non-specific binding to brain lipids rather than free drug levels. As the complex nature of the brain requires different compartments to be considered when trying to understand and improve new compounds, several complementary parameters need to be measured in vitro and in vivo, and integrated into a coherent model of brain penetration and distribution.
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    Malon V. Kootstra 1 , Charlotte E. Teunissen 4 , Ron Mathot 1 , Dasja Pajkrt 2. Despite optimal responses to combination antiretroviral therapy cART , HIV-infected children continue to show neurocognitive deficits with macro- and microstructural brain injury and signs of neuroinflammation. Subtherapeutic central nervous system CNS drug levels may contribute to neuropathology in these children.
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