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Article ; Online: Discovery of vimseltinib (DCC-3014), a highly selective CSF1R switch-control kinase inhibitor, in clinical development for the treatment of Tenosynovial Giant Cell Tumor (TGCT).

Caldwell, Timothy M / Ahn, Yu Mi / Bulfer, Stacie L / Leary, Cynthia B / Hood, Molly M / Lu, Wei-Ping / Vogeti, Lakshminarayana / Vogeti, Subha / Kaufman, Michael D / Wise, Scott C / Le Bourdonnec, Bertrand / Smith, Bryan D / Flynn, Daniel L

Bioorganic & medicinal chemistry letters

2022 Volume 74, Page(s) 128928

Abstract: Based on knowledge of kinase switch-control inhibition and using a combination of structure-based drug design and standard medicinal chemistry principles, we identified a novel series of dihydropyrimidone-based CSF1R kinase inhibitors displaying ... ...

Abstract	Based on knowledge of kinase switch-control inhibition and using a combination of structure-based drug design and standard medicinal chemistry principles, we identified a novel series of dihydropyrimidone-based CSF1R kinase inhibitors displaying exquisite selectivity for CSF1R versus a large panel of kinases and non-kinase protein targets. Starting with lead compound 3, an SAR optimization campaign led to the discovery of vimseltinib (DCC-3014; compound 20) currently undergoing clinical evaluation for the treatment of Tenosynovial Giant Cell Tumor (TGCT), a locally aggressive benign tumor associated with substantial morbidity. 2021 Elsevier ltd. All rights reserved.
MeSH term(s)	Antineoplastic Agents/pharmacology ; Antineoplastic Agents/therapeutic use ; DCC Receptor ; Giant Cell Tumor of Tendon Sheath/drug therapy ; Giant Cell Tumor of Tendon Sheath/pathology ; Humans ; Protein Kinase Inhibitors/pharmacology ; Protein Kinase Inhibitors/therapeutic use ; Receptor Protein-Tyrosine Kinases ; Receptor, Macrophage Colony-Stimulating Factor
Chemical Substances	Antineoplastic Agents ; DCC Receptor ; DCC protein, human ; Protein Kinase Inhibitors ; Receptor Protein-Tyrosine Kinases (EC 2.7.10.1) ; Receptor, Macrophage Colony-Stimulating Factor (EC 2.7.10.1)
Language	English
Publishing date	2022-08-10
Publishing country	England
Document type	Journal Article
ZDB-ID	1063195-1
ISSN	1464-3405 ; 0960-894X
ISSN (online)	1464-3405
ISSN	0960-894X
DOI	10.1016/j.bmcl.2022.128928
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Article ; Online: Discovery of acyl ureas as highly selective small molecule CSF1R kinase inhibitors.

Caldwell, Timothy M / Kaufman, Michael D / Wise, Scott C / Mi Ahn, Yu / Hood, Molly M / Lu, Wei-Ping / Patt, William C / Samarakoon, Thiwanka / Vogeti, Lakshminarayana / Vogeti, Subha / Yates, Karen M / Bulfer, Stacie L / Le Bourdonnec, Bertrand / Smith, Bryan D / Flynn, Daniel L

Bioorganic & medicinal chemistry letters

2022 Volume 74, Page(s) 128929

Abstract: Based on the structure of an early lead identified in Deciphera's proprietary compound collection of switch control kinase inhibitors and using a combination of medicinal chemistry guided structure activity relationships and structure-based drug design, ... ...

Abstract	Based on the structure of an early lead identified in Deciphera's proprietary compound collection of switch control kinase inhibitors and using a combination of medicinal chemistry guided structure activity relationships and structure-based drug design, a novel series of potent acyl urea-based CSF1R inhibitors was identified displaying high selectivity for CSF1R versus the other members of the Type III receptor tyrosine kinase (RTK) family members (KIT, PDGFR-α, PDGFR-β, and FLT3), VEGFR2 and MET. Based on in vitro biology, in vitro ADME and in vivo PK/PD studies, compound 10 was selected as an advanced lead for Deciphera's CSF1R research program.
MeSH term(s)	Drug Design ; Protein Kinase Inhibitors/chemistry ; Protein Kinase Inhibitors/pharmacology ; Receptor Protein-Tyrosine Kinases ; Receptor, Platelet-Derived Growth Factor beta ; Structure-Activity Relationship ; Urea/chemistry ; Urea/pharmacology
Chemical Substances	Protein Kinase Inhibitors ; Urea (8W8T17847W) ; Receptor Protein-Tyrosine Kinases (EC 2.7.10.1) ; Receptor, Platelet-Derived Growth Factor beta (EC 2.7.10.1)
Language	English
Publishing date	2022-08-09
Publishing country	England
Document type	Journal Article
ZDB-ID	1063195-1
ISSN	1464-3405 ; 0960-894X
ISSN (online)	1464-3405
ISSN	0960-894X
DOI	10.1016/j.bmcl.2022.128929
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Article ; Online: Course of relapsing-remitting multiple sclerosis before, during and after natalizumab.

Kaufman, Michael D / Lee, R / Norton, H J

Multiple sclerosis (Houndmills, Basingstoke, England)

2011 Volume 17, Issue 4, Page(s) 490–494

Abstract: The consequences of interruption of natalizumab treatment are incompletely known. The objective was to assess the confirmed annualized relapse rates for patients preceding initiation, during and following suspension of natalizumab therapy. A chart review ...

Abstract	The consequences of interruption of natalizumab treatment are incompletely known. The objective was to assess the confirmed annualized relapse rates for patients preceding initiation, during and following suspension of natalizumab therapy. A chart review was conducted and data were analyzed using the Generalized Estimating Equations. During natalizumab therapy the confirmed annualized relapse rate was 0.08, compared to 0.52 (p = 0.0003) during the prior 12 months and to 0.35 (p = 0.0032) during the following 3 to 24 months. Similar results were found when confirmed and unconfirmed were analyzed. To conclude, following cessation of natalizumab therapy disease activity rapidly returned to pre-natalizumab levels.
MeSH term(s)	Antibodies, Monoclonal/therapeutic use ; Antibodies, Monoclonal, Humanized ; Disease Progression ; Female ; Humans ; Male ; Multiple Sclerosis, Relapsing-Remitting/therapy ; Natalizumab ; Recurrence
Chemical Substances	Antibodies, Monoclonal ; Antibodies, Monoclonal, Humanized ; Natalizumab
Language	English
Publishing date	2011-04
Publishing country	England
Document type	Journal Article
ZDB-ID	1290669-4
ISSN	1477-0970 ; 1352-4585
ISSN (online)	1477-0970
ISSN	1352-4585
DOI	10.1177/1352458510389103
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Zs.A 4428: Show issues

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Article ; Online: Vimseltinib: A Precision CSF1R Therapy for Tenosynovial Giant Cell Tumors and Diseases Promoted by Macrophages.

Smith, Bryan D / Kaufman, Michael D / Wise, Scott C / Ahn, Yu Mi / Caldwell, Timothy M / Leary, Cynthia B / Lu, Wei-Ping / Tan, Gege / Vogeti, Lakshminarayana / Vogeti, Subha / Wilky, Breelyn A / Davis, Lara E / Sharma, Maitreyi / Ruiz-Soto, Rodrigo / Flynn, Daniel L

Molecular cancer therapeutics

2021 Volume 20, Issue 11, Page(s) 2098–2109

Abstract: Macrophages can be co-opted to contribute to neoplastic, neurologic, and inflammatory diseases. Colony-stimulating factor 1 receptor (CSF1R)-dependent macrophages and other inflammatory cells can suppress the adaptive immune system in cancer and ... ...

Abstract	Macrophages can be co-opted to contribute to neoplastic, neurologic, and inflammatory diseases. Colony-stimulating factor 1 receptor (CSF1R)-dependent macrophages and other inflammatory cells can suppress the adaptive immune system in cancer and contribute to angiogenesis, tumor growth, and metastasis. CSF1R-expressing osteoclasts mediate bone degradation in osteolytic cancers and cancers that metastasize to bone. In the rare disease tenosynovial giant cell tumor (TGCT), aberrant CSF1 expression and production driven by a gene translocation leads to the recruitment and growth of tumors formed by CSF1R-dependent inflammatory cells. Small molecules and antibodies targeting the CSF1/CSF1R axis have shown promise in the treatment of TGCT and cancer, with pexidartinib recently receiving FDA approval for treatment of TGCT. Many small-molecule kinase inhibitors of CSF1R also inhibit the closely related kinases KIT, PDGFRA, PDGFRB, and FLT3, thus CSF1R suppression may be limited by off-target activity and associated adverse events. Vimseltinib (DCC-3014) is an oral, switch control tyrosine kinase inhibitor specifically designed to selectively and potently inhibit CSF1R by exploiting unique features of the switch control region that regulates kinase conformational activation. In preclinical studies, vimseltinib durably suppressed CSF1R activity
MeSH term(s)	Adult ; Animals ; Cell Proliferation ; Cross-Over Studies ; Disease Models, Animal ; Female ; Giant Cell Tumor of Tendon Sheath/drug therapy ; Humans ; Macrophages/drug effects ; Male ; Mice ; Mice, Nude ; Middle Aged ; Models, Molecular ; Protein Kinase Inhibitors/pharmacology ; Protein Kinase Inhibitors/therapeutic use ; Rats ; Rats, Sprague-Dawley ; Young Adult
Chemical Substances	Protein Kinase Inhibitors
Language	English
Publishing date	2021-08-25
Publishing country	United States
Document type	Case Reports ; Journal Article ; Research Support, Non-U.S. Gov't
ZDB-ID	2063563-1
ISSN	1538-8514 ; 1535-7163
ISSN (online)	1538-8514
ISSN	1535-7163
DOI	10.1158/1535-7163.MCT-21-0361
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Article ; Online: Double-lumen tubes: which lumen for the gum elastic bougie?

Stix, Michael S / Ata, Sana / Wolckenhaar, Marten / Kaufman, Michael D

Anesthesia and analgesia

2010 Volume 110, Issue 1, Page(s) 258; author reply 258–9

MeSH term(s)	Humans ; Intubation, Intratracheal/instrumentation ; Intubation, Intratracheal/methods ; Laryngoscopes ; Optical Fibers ; Trachea/anatomy & histology
Language	English
Publishing date	2010-01-01
Publishing country	United States
Document type	Comment ; Letter
ZDB-ID	80032-6
ISSN	1526-7598 ; 0003-2999
ISSN (online)	1526-7598
ISSN	0003-2999
DOI	10.1213/ANE.0b013e3181c293cf
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Article ; Online: A Phase I Study of LY3009120, a Pan-RAF Inhibitor, in Patients with Advanced or Metastatic Cancer.

Molecular cancer therapeutics

2019 Volume 19, Issue 2, Page(s) 460–467

Abstract: Mutations in ERK signaling drive a significant percentage of malignancies. LY3009120, a pan-RAF and dimer inhibitor, has preclinical activity ... ...

Abstract	Mutations in ERK signaling drive a significant percentage of malignancies. LY3009120, a pan-RAF and dimer inhibitor, has preclinical activity in
MeSH term(s)	Adult ; Aged ; Aged, 80 and over ; Cell Line, Tumor ; Female ; Humans ; Male ; Middle Aged ; Neoplasm Metastasis ; Neoplasms/drug therapy ; Phenylurea Compounds/pharmacology ; Phenylurea Compounds/therapeutic use ; Pyrimidines/pharmacology ; Pyrimidines/therapeutic use ; Young Adult
Chemical Substances	LY3009120 ; Phenylurea Compounds ; Pyrimidines
Language	English
Publishing date	2019-10-23
Publishing country	United States
Document type	Clinical Trial, Phase I ; Journal Article ; Multicenter Study ; Research Support, Non-U.S. Gov't
ZDB-ID	2063563-1
ISSN	1538-8514 ; 1535-7163
ISSN (online)	1538-8514
ISSN	1535-7163
DOI	10.1158/1535-7163.MCT-19-0681
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Article: Adherence to therapy: using an evidence-based protocol.

Moore, Linda A / Kaufman, Michael D / Algozzine, Robert / Irish, Nikki / Martin, Mary / Posey, Carol Rosser

Rehabilitation nursing : the official journal of the Association of Rehabilitation Nurses

2007 Volume 32, Issue 6, Page(s) 227–232

Abstract: The number of patients receiving injectable medications has increased significantly during the past few years. Today, patients with hepatitis, rheumatoid arthritis, and multiple sclerosis are added to the list of those, namely diabetics, who have been ... ...

Abstract	The number of patients receiving injectable medications has increased significantly during the past few years. Today, patients with hepatitis, rheumatoid arthritis, and multiple sclerosis are added to the list of those, namely diabetics, who have been instructed in self-administration of injectable medications. Currently, some of these medications create significant skin site reactions, and patients tend to discontinue the medications without informing the healthcare provider. Determining the problem and developing a research study that provides evidence to demonstrate methods to help patients adhere to agreed-upon treatment modalities can be accomplished within the clinical practice setting. This study provided a method to decrease skin reactions with interferon 1-b injections for multiple sclerosis patients and has been continued as a method with other like medications.
MeSH term(s)	Adjuvants, Immunologic/administration & dosage ; Adjuvants, Immunologic/adverse effects ; Adult ; Air ; Clinical Nursing Research ; Clinical Protocols ; Cross-Over Studies ; Erythema/chemically induced ; Erythema/diagnosis ; Erythema/prevention & control ; Evidence-Based Medicine ; Female ; Humans ; Injections, Intramuscular/adverse effects ; Injections, Intramuscular/methods ; Injections, Intramuscular/psychology ; Interferon beta-1b ; Interferon-beta/administration & dosage ; Interferon-beta/adverse effects ; Male ; Middle Aged ; Multiple Sclerosis/drug therapy ; Multiple Sclerosis/psychology ; Nurse's Role ; Nursing Assessment ; Nursing Methodology Research ; Patient Compliance/psychology ; Patient Education as Topic ; Self Administration/adverse effects ; Self Administration/methods ; Self Administration/psychology ; Skin Temperature ; Surveys and Questionnaires
Chemical Substances	Adjuvants, Immunologic ; Interferon beta-1b (145155-23-3) ; Interferon-beta (77238-31-4)
Language	English
Publishing date	2007-12-05
Publishing country	United States
Document type	Journal Article ; Randomized Controlled Trial
ZDB-ID	604872-9
ISSN	0278-4807 ; 0248-7940
ISSN	0278-4807 ; 0248-7940
DOI	10.1002/j.2048-7940.2007.tb00179.x
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Article ; Online: Ripretinib (DCC-2618) Is a Switch Control Kinase Inhibitor of a Broad Spectrum of Oncogenic and Drug-Resistant KIT and PDGFRA Variants.

Smith, Bryan D / Kaufman, Michael D / Lu, Wei-Ping / Gupta, Anu / Leary, Cynthia B / Wise, Scott C / Rutkoski, Thomas J / Ahn, Yu Mi / Al-Ani, Gada / Bulfer, Stacie L / Caldwell, Timothy M / Chun, Lawrence / Ensinger, Carol L / Hood, Molly M / McKinley, Arin / Patt, William C / Ruiz-Soto, Rodrigo / Su, Ying / Telikepalli, Hanumaiah /

Town, Ajia / Turner, Benjamin A / Vogeti, Lakshminarayana / Vogeti, Subha / Yates, Karen / Janku, Filip / Abdul Razak, Albiruni Ryan / Rosen, Oliver / Heinrich, Michael C / Flynn, Daniel L

Cancer cell

2019 Volume 35, Issue 5, Page(s) 738–751.e9

Abstract: Ripretinib (DCC-2618) was designed to inhibit the full spectrum of mutant KIT and PDGFRA kinases found in cancers and myeloproliferative neoplasms, particularly in gastrointestinal stromal tumors (GISTs), in which the heterogeneity of drug-resistant KIT ... ...

Abstract	Ripretinib (DCC-2618) was designed to inhibit the full spectrum of mutant KIT and PDGFRA kinases found in cancers and myeloproliferative neoplasms, particularly in gastrointestinal stromal tumors (GISTs), in which the heterogeneity of drug-resistant KIT mutations is a major challenge. Ripretinib is a "switch-control" kinase inhibitor that forces the activation loop (or activation "switch") into an inactive conformation. Ripretinib inhibits all tested KIT and PDGFRA mutants, and notably is a type II kinase inhibitor demonstrated to broadly inhibit activation loop mutations in KIT and PDGFRA, previously thought only achievable with type I inhibitors. Ripretinib shows efficacy in preclinical cancer models, and preliminary clinical data provide proof-of-concept that ripretinib inhibits a wide range of KIT mutants in patients with drug-resistant GISTs.
MeSH term(s)	Animals ; Antineoplastic Agents/pharmacology ; CHO Cells ; Cell Line ; Cell Line, Tumor ; Cricetulus ; Drug Resistance, Neoplasm/drug effects ; Drug Resistance, Neoplasm/genetics ; Gastrointestinal Neoplasms/drug therapy ; Gastrointestinal Neoplasms/genetics ; HCT116 Cells ; Human Umbilical Vein Endothelial Cells ; Humans ; Mice ; Mice, Inbred BALB C ; Mice, Inbred NOD ; Mice, Nude ; Mice, SCID ; Mutation/drug effects ; Mutation/genetics ; Protein Kinase Inhibitors/pharmacology ; Proto-Oncogene Proteins c-kit/genetics ; Receptor, Platelet-Derived Growth Factor alpha/genetics
Chemical Substances	Antineoplastic Agents ; Protein Kinase Inhibitors ; KIT protein, human (EC 2.7.10.1) ; Proto-Oncogene Proteins c-kit (EC 2.7.10.1) ; Receptor, Platelet-Derived Growth Factor alpha (EC 2.7.10.1)
Language	English
Publishing date	2019-05-03
Publishing country	United States
Document type	Journal Article
ZDB-ID	2078448-X
ISSN	1878-3686 ; 1535-6108
ISSN (online)	1878-3686
ISSN	1535-6108
DOI	10.1016/j.ccell.2019.04.006
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Zs.A 5650: Show issues			Location: Je nach Verfügbarkeit (siehe Angabe bei Bestand) bis Jg. 1994: Bestellungen von Artikeln über das Online-Bestellformular Jg. 1995 - 2021: Lesesall (2.OG) ab Jg. 2022: Lesesaal (EG)
Zs.MG 104: Show issues

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Article ; Online: The Selective Tie2 Inhibitor Rebastinib Blocks Recruitment and Function of Tie2

Molecular cancer therapeutics

2017 Volume 16, Issue 11, Page(s) 2486–2501

Abstract: Tumor-infiltrating myeloid cells promote tumor progression by mediating angiogenesis, tumor cell intravasation, and metastasis, which can offset the effects of chemotherapy, radiation, and antiangiogenic therapy. Here, we show that the kinase switch ... ...

Abstract	Tumor-infiltrating myeloid cells promote tumor progression by mediating angiogenesis, tumor cell intravasation, and metastasis, which can offset the effects of chemotherapy, radiation, and antiangiogenic therapy. Here, we show that the kinase switch control inhibitor rebastinib inhibits Tie2, a tyrosine kinase receptor expressed on endothelial cells and protumoral Tie2-expressing macrophages in mouse models of metastatic cancer. Rebastinib reduces tumor growth and metastasis in an orthotopic mouse model of metastatic mammary carcinoma through reduction of Tie2
MeSH term(s)	Angiopoietins/antagonists & inhibitors ; Angiopoietins/genetics ; Animals ; Breast Neoplasms/drug therapy ; Breast Neoplasms/genetics ; Breast Neoplasms/pathology ; Cell Line, Tumor ; Cell Proliferation/drug effects ; Female ; Humans ; Macrophages/drug effects ; Mice ; Neovascularization, Pathologic/drug therapy ; Neovascularization, Pathologic/genetics ; Neovascularization, Pathologic/pathology ; Neuroendocrine Tumors/drug therapy ; Neuroendocrine Tumors/genetics ; Neuroendocrine Tumors/pathology ; Pancreatic Neoplasms/drug therapy ; Pancreatic Neoplasms/genetics ; Pancreatic Neoplasms/pathology ; Pyrazoles/pharmacology ; Pyrazoles/therapeutic use ; Pyridines/pharmacology ; Pyridines/therapeutic use ; Quinolines/pharmacology ; Quinolines/therapeutic use ; Receptor, TIE-2/antagonists & inhibitors ; Receptor, TIE-2/genetics ; Signal Transduction/drug effects ; Tumor Microenvironment/drug effects
Chemical Substances	Angiopoietins ; Pyrazoles ; Pyridines ; Quinolines ; rebastinib (75017Q6I97) ; Receptor, TIE-2 (EC 2.7.10.1)
Language	English
Publishing date	2017-08-24
Publishing country	United States
Document type	Journal Article ; Research Support, N.I.H., Extramural ; Research Support, Non-U.S. Gov't ; Research Support, U.S. Gov't, Non-P.H.S.
ZDB-ID	2063563-1
ISSN	1538-8514 ; 1535-7163
ISSN (online)	1538-8514
ISSN	1535-7163
DOI	10.1158/1535-7163.MCT-17-0241
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Article: Multiple sclerosis: severity and progression rate in African Americans compared with whites.

Kaufman, Michael D / Johnson, Susan K / Moyer, David / Bivens, Jessica / Norton, H James

American journal of physical medicine & rehabilitation

2003 Volume 82, Issue 8, Page(s) 582–590

Abstract: Objective: Although epidemiology indicates that multiple sclerosis is more common among whites than African Americans, the course of disease may be more aggressive among African Americans. This study examines disease course in a large multiple sclerosis ...

Abstract	Objective: Although epidemiology indicates that multiple sclerosis is more common among whites than African Americans, the course of disease may be more aggressive among African Americans. This study examines disease course in a large multiple sclerosis clinic population. Design: A case-controlled, retrospective record review compared the severity of multiple sclerosis for African Americans and for whites. Because the baseline demographics of the two groups differed, we performed analyses of multiple subgroups in an attempt to control for various characteristics. Results: Consistent evidence of more disability in African Americans compared with whites was found, although subgroups were often too small to establish statistical significance. African Americans had a higher mean Expanded Disability Status Scale score than whites in a subgroup selected to minimize differences in access to care and disease perceptions. African Americans reported limb weakness as a presenting symptom of multiple sclerosis more frequently than did whites. When patients were followed at our multiple sclerosis center, rates of disease progression were nearly identical. Conclusions: More African Americans than whites experience pyramidal system involvement early in multiple sclerosis, leading to greater disability as measured by the ambulation-sensitive Expanded Disability Status Scale. Once patients have moderate difficulty walking, the rate of progression is the same for both groups, albeit occurring at a later age for whites than for African Americans.
MeSH term(s)	Adult ; African Continental Ancestry Group ; Disability Evaluation ; European Continental Ancestry Group ; Female ; Humans ; Male ; Middle Aged ; Multiple Sclerosis/classification ; Multiple Sclerosis/epidemiology ; Multiple Sclerosis/mortality ; North Carolina/epidemiology ; Population Surveillance ; Retrospective Studies ; Severity of Illness Index
Language	English
Publishing date	2003-08
Publishing country	United States
Document type	Comparative Study ; Journal Article
ZDB-ID	219390-5
ISSN	1537-7385 ; 0894-9115 ; 0002-9491
ISSN (online)	1537-7385
ISSN	0894-9115 ; 0002-9491
DOI	10.1097/01.PHM.0000078199.99484.E2
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