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Evidence supporting that the attribution of first success in use of arsenic for the treatment of leukaemia should be to David Lissauer (1836–1892)

Leukemia, 2022-06, Vol.36 (6), p.1697-1698

Manley, Paul W.

2022

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The specificity of asciminib, a potential treatment for chronic myeloid leukemia, as a myristate-pocket binding ABL inhibitor and analysis of its interactions with mutant forms of BCR-ABL1 kinase

Leukemia research, 2020-11, Vol.98, p.106458, Article 106458

2020

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Discovery of Asciminib (ABL001), an Allosteric Inhibitor of the Tyrosine Kinase Activity of BCR-ABL1

Journal of medicinal chemistry, 2018-09, Vol.61 (18), p.8120-8135

2018

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Imaging the intracellular distribution of tyrosine kinase inhibitors in living cells with quantitative hyperspectral stimulated Raman scattering

Nature chemistry, 2014-07, Vol.6 (7), p.614-622

2014

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Investigations into the Potential Role of Metabolites on the Anti-Leukemic Activity of Imatinib, Nilotinib and Midostaurin

Chimia, 2019-08, Vol.73 (7-8), p.561

Manley, Paul W

2019

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Acute-phase serum amyloid A: Perspectives on its physiological and pathological roles

Amyloid, 2012-03, Vol.19 (1), p.5-14

2012

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Midostaurin: its odyssey from discovery to approval for treating acute myeloid leukemia and advanced systemic mastocytosis

Blood advances, 2018-02, Vol.2 (4), p.444-453

2018

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A kinase inhibitor which specifically targets the ABL myristate pocket (STAMP), but unlike asciminib crosses the blood–brain barrier

Bioorganic & medicinal chemistry letters, 2022-03, Vol.59, p.128577-128577, Article 128577

2022

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Inhibition of collagen-induced discoidin domain receptor 1 and 2 activation by imatinib, nilotinib and dasatinib

European journal of pharmacology, 2008-12, Vol.599 (1), p.44-53

2008

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Second generation inhibitors of BCR-ABL for the treatment of imatinib-resistant chronic myeloid leukaemia

Nature reviews. Cancer, 2007-05, Vol.7 (5), p.345-356

2007

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Comparison of the Kinase Profile of Midostaurin (Rydapt) with That of Its Predominant Metabolites and the Potential Relevance of Some Newly Identified Targets to Leukemia Therapy

Biochemistry (Easton), 2018-09, Vol.57 (38), p.5576-5590

2018

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Characterization of AMN107, a selective inhibitor of native and mutant Bcr-Abl

Cancer cell, 2005-02, Vol.7 (2), p.129-141

2005

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Evidence that resistance to nilotinib may be due to BCR-ABL, Pgp, or Src kinase overexpression

Cancer research (Chicago, Ill.), 2008-12, Vol.68 (23), p.9809-9816

2008

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Most CML patients who have a suboptimal response to imatinib have low OCT-1 activity: higher doses of imatinib may overcome the negative impact of low OCT-1 activity

Blood, 2007-12, Vol.110 (12), p.4064-4072

2007

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In vitro activity of Bcr-Abl inhibitors AMN107 and BMS-354825 against clinically relevant imatinib-resistant Abl kinase domain mutants

Cancer research (Chicago, Ill.), 2005-06, Vol.65 (11), p.4500-4505

2005

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Expansion of Bcr-Abl-Positive Leukemic Stem Cells Is Dependent on Hedgehog Pathway Activation

Cancer cell, 2008-09, Vol.14 (3), p.238-249

2008

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Functional Activity of the OCT-1 Protein Is Predictive of Long-Term Outcome in Patients With Chronic-Phase Chronic Myeloid Leukemia Treated With Imatinib

Journal of clinical oncology, 2010-06, Vol.28 (16), p.2761-2767

2010

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Structural resemblances and comparisons of the relative pharmacological properties of imatinib and nilotinib

Bioorganic & medicinal chemistry, 2010-10, Vol.18 (19), p.6977-6986

2010

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The kinetic deuterium isotope effect as applied to metabolic deactivation of imatinib to the des-methyl metabolite, CGP74588

Bioorganic & medicinal chemistry, 2013-06, Vol.21 (11), p.3231-3239

2013

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Correspondence on “Synergy and Antagonism between Allosteric and Active‐Site Inhibitors of Abl Tyrosine Kinase”

Angewandte Chemie International Edition, 2022-11, Vol.61 (46), p.e202117276-n/a

International ed. in English, 2022

Volltextzugriff (PDF)

Solution Conformations and Dynamics of ABL Kinase-Inhibitor Complexes Determined by NMR Substantiate the Different Binding Modes of Imatinib/Nilotinib and Dasatinib

The Journal of biological chemistry, 2008-06, Vol.283 (26), p.18292-18302

2008

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The Crystal Structure of a c-Src Complex in an Active Conformation Suggests Possible Steps in c-Src Activation

Structure (London), 2005-06, Vol.13 (6), p.861-871

2005

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Familial PDGFRA-mutation syndrome: somatic and gastrointestinal phenotype

Human pathology, 2018-06, Vol.76, p.52-57

2018

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Targeting Bcr-Abl by combining allosteric with ATP-binding-site inhibitors

Nature (London), 2010-01, Vol.463 (7280), p.501-506

2010

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Extended kinase profile and properties of the protein kinase inhibitor nilotinib

Biochimica et biophysica acta, 2010-03, Vol.1804 (3), p.445-453

2010

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Evidence supporting that the attribution of first success in use of arsenic for the treatment of leukaemia should be to David Lissauer (1836–1892)

The specificity of asciminib, a potential treatment for chronic myeloid leukemia, as a myristate-pocket binding ABL inhibitor and analysis of its interactions with mutant forms of BCR-ABL1 kinase

Discovery of Asciminib (ABL001), an Allosteric Inhibitor of the Tyrosine Kinase Activity of BCR-ABL1

Imaging the intracellular distribution of tyrosine kinase inhibitors in living cells with quantitative hyperspectral stimulated Raman scattering

Investigations into the Potential Role of Metabolites on the Anti-Leukemic Activity of Imatinib, Nilotinib and Midostaurin

Acute-phase serum amyloid A: Perspectives on its physiological and pathological roles

Midostaurin: its odyssey from discovery to approval for treating acute myeloid leukemia and advanced systemic mastocytosis

A kinase inhibitor which specifically targets the ABL myristate pocket (STAMP), but unlike asciminib crosses the blood–brain barrier

Inhibition of collagen-induced discoidin domain receptor 1 and 2 activation by imatinib, nilotinib and dasatinib

Second generation inhibitors of BCR-ABL for the treatment of imatinib-resistant chronic myeloid leukaemia

Comparison of the Kinase Profile of Midostaurin (Rydapt) with That of Its Predominant Metabolites and the Potential Relevance of Some Newly Identified Targets to Leukemia Therapy

Characterization of AMN107, a selective inhibitor of native and mutant Bcr-Abl

Evidence that resistance to nilotinib may be due to BCR-ABL, Pgp, or Src kinase overexpression

Most CML patients who have a suboptimal response to imatinib have low OCT-1 activity: higher doses of imatinib may overcome the negative impact of low OCT-1 activity

In vitro activity of Bcr-Abl inhibitors AMN107 and BMS-354825 against clinically relevant imatinib-resistant Abl kinase domain mutants

Expansion of Bcr-Abl-Positive Leukemic Stem Cells Is Dependent on Hedgehog Pathway Activation

Functional Activity of the OCT-1 Protein Is Predictive of Long-Term Outcome in Patients With Chronic-Phase Chronic Myeloid Leukemia Treated With Imatinib

Structural resemblances and comparisons of the relative pharmacological properties of imatinib and nilotinib

The kinetic deuterium isotope effect as applied to metabolic deactivation of imatinib to the des-methyl metabolite, CGP74588

Correspondence on “Synergy and Antagonism between Allosteric and Active‐Site Inhibitors of Abl Tyrosine Kinase”

Solution Conformations and Dynamics of ABL Kinase-Inhibitor Complexes Determined by NMR Substantiate the Different Binding Modes of Imatinib/Nilotinib and Dasatinib

The Crystal Structure of a c-Src Complex in an Active Conformation Suggests Possible Steps in c-Src Activation

Familial PDGFRA-mutation syndrome: somatic and gastrointestinal phenotype

Targeting Bcr-Abl by combining allosteric with ATP-binding-site inhibitors

Extended kinase profile and properties of the protein kinase inhibitor nilotinib

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