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We began analyzing https://link.springer.com/article/10.1007/s00280-014-2530-9, but it redirected us to https://link.springer.com/article/10.1007/s00280-014-2530-9. The analysis below is for the second page.

Title[redir]:
Mechanism-based pharmacokinetic/pharmacodynamic meta-analysis of navitoclax (ABT-263) induced thrombocytopenia | Cancer Chemotherapy and Pharmacology
Description:
Objective Navitoclax is a first-in-class, orally bioavailable, targeted Bcl-2 family protein inhibitor and promotes apoptosis. Thrombocytopenia is a primary dose-limiting toxicity of navitoclax which exhibited a distinct time profile in circulating platelets from that caused by traditional chemotherapies. A population pharmacokinetic/pharmacodynamic (PK/PD) model was developed to describe the pharmacokinetic of navitoclax as well as the time course of the platelet counts in cancer patients receiving navitoclax. Methods Data from 256 patients who received oral navitoclax (dose range 10–475 mg) as a 14/21-day schedule or a continuous once daily (QD) schedule were used to construct the model using NONMEM. The PK model was a two-compartmental model with a lag-time and a transit compartment in absorption. The PD model was a semi-physiological model that comprised a progenitor cell compartment, three transition compartments representing the maturation chain in the bone marrow and a peripheral blood compartment. Compared with the previously published models, the model established in this analysis applied a different feedback mechanism and introduced a new concept of progenitor cell “pool”, which describes a large pool of platelet progenitor cells at the beginning of navitoclax treatment. Results The PD model was able to describe a slight downward trend of platelet counts over the long-term navitoclax treatment as observed in around 8 % of the patients and the initial drop in platelets seen in our Phase 1/2a studies. Conclusions We have developed a new semi-physiological platelet model for describing fast drop of platelets after initial navitoclax administration and long-term decline of platelets after continuous administration of navitoclax.

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Keywords {🔍}

navitoclax, article, model, cancer, patients, study, abt, bcl, phase, pubmed, google, scholar, xiong, platelet, oncol, cas, abbvie, privacy, cookies, content, data, pharmacology, kaefer, yang, humerickhouse, family, inhibitor, cell, clin, publish, research, search, thrombocytopenia, aksana, noertersheuser, platelets, results, access, chronic, lymphocytic, leukemia, analysis, information, log, journal, pharmacokineticpharmacodynamic, published, july, jianning, peter,

Topics {✒️}

mechanism-based pharmacokinetic/pharmacodynamic meta-analysis small-cell lung cancer month download article/chapter targeted high-affinity inhibitor holland-frei cancer medicine nanoparticle albumin-bound paclitaxel primary dose-limiting toxicity phase ii open-label population pharmacokinetic/pharmacodynamic semi-mechanistic myelosuppression model semi-physiological platelet model previously untreated advanced article cancer chemotherapy chronic lymphocytic leukemia related subjects long-term navitoclax treatment full article pdf previously published models privacy choices/manage cookies bcl-2 family inhibitor chemotherapy-induced myelosuppression walid awni progenitor cell compartment progenitor cell “pool” tumour cell survival bcl-2 family proteins semi-physiological model long-term decline platelet progenitor cells dose range 10–475 mg pharmacology aims clinical pharmacology european economic area transition compartments representing slight downward trend ribeiro de oliveira conditions privacy policy peripheral blood compartment describing fast drop hao xiong phase 1/2a studies received oral navitoclax bast jr rc accepting optional cookies solid tumors friberg le induced thrombocytopenia article kaefer phase ii study distinct time profile

Schema {🗺️}

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