Ahmed Hamdy
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View article: Enitociclib, a selective CDK9 inhibitor: in vitro and in vivo preclinical studies in multiple myeloma
Enitociclib, a selective CDK9 inhibitor: in vitro and in vivo preclinical studies in multiple myeloma Open
View article: Neutrophil elastase as a versatile cleavage enzyme for activation of αvβ3 integrin-targeted small molecule drug conjugates with different payload classes in the tumor microenvironment
Neutrophil elastase as a versatile cleavage enzyme for activation of αvβ3 integrin-targeted small molecule drug conjugates with different payload classes in the tumor microenvironment Open
Introduction: The development of bioconjugates for the targeted delivery of anticancer agents is gaining momentum after recent success of antibody drug conjugates (ADCs) in the clinic. Smaller format conjugates may have several advantages …
View article: Fig S5 from Pharmacodynamic Analysis of BTK Inhibition in Patients with Chronic Lymphocytic Leukemia Treated with Acalabrutinib
Fig S5 from Pharmacodynamic Analysis of BTK Inhibition in Patients with Chronic Lymphocytic Leukemia Treated with Acalabrutinib Open
Rate of change in percent free BTK per day.
View article: Data from Pharmacodynamic Analysis of BTK Inhibition in Patients with Chronic Lymphocytic Leukemia Treated with Acalabrutinib
Data from Pharmacodynamic Analysis of BTK Inhibition in Patients with Chronic Lymphocytic Leukemia Treated with Acalabrutinib Open
Purpose:To determine the pharmacodynamic relationship between target occupancy of Bruton tyrosine kinase (BTK) and inhibition of downstream signaling.Patients and Methods:Patients with chronic lymphocytic leukemia (CLL) enrolled in a phase…
View article: Table S3 from Pharmacodynamic Analysis of BTK Inhibition in Patients with Chronic Lymphocytic Leukemia Treated with Acalabrutinib
Table S3 from Pharmacodynamic Analysis of BTK Inhibition in Patients with Chronic Lymphocytic Leukemia Treated with Acalabrutinib Open
Supplementary Table S3: List of patients included in the analysis of rebound in cellular signaling during drug withholding
View article: Fig S2 from Pharmacodynamic Analysis of BTK Inhibition in Patients with Chronic Lymphocytic Leukemia Treated with Acalabrutinib
Fig S2 from Pharmacodynamic Analysis of BTK Inhibition in Patients with Chronic Lymphocytic Leukemia Treated with Acalabrutinib Open
Flow cytometry gating strategy for CD69.
View article: Fig S2 from Pharmacodynamic Analysis of BTK Inhibition in Patients with Chronic Lymphocytic Leukemia Treated with Acalabrutinib
Fig S2 from Pharmacodynamic Analysis of BTK Inhibition in Patients with Chronic Lymphocytic Leukemia Treated with Acalabrutinib Open
Flow cytometry gating strategy for CD69.
View article: Table S2 from Pharmacodynamic Analysis of BTK Inhibition in Patients with Chronic Lymphocytic Leukemia Treated with Acalabrutinib
Table S2 from Pharmacodynamic Analysis of BTK Inhibition in Patients with Chronic Lymphocytic Leukemia Treated with Acalabrutinib Open
Supplementary Table S2: Assay IDs for genes analyzed by RT-PCR
View article: Fig S3 from Pharmacodynamic Analysis of BTK Inhibition in Patients with Chronic Lymphocytic Leukemia Treated with Acalabrutinib
Fig S3 from Pharmacodynamic Analysis of BTK Inhibition in Patients with Chronic Lymphocytic Leukemia Treated with Acalabrutinib Open
Flow cytometry gating strategy for pBTK after in vitro stimulation.
View article: Fig S4 from Pharmacodynamic Analysis of BTK Inhibition in Patients with Chronic Lymphocytic Leukemia Treated with Acalabrutinib
Fig S4 from Pharmacodynamic Analysis of BTK Inhibition in Patients with Chronic Lymphocytic Leukemia Treated with Acalabrutinib Open
Flow cytometry gating strategy for CD69 after in vitro stimulation.
View article: Fig S5 from Pharmacodynamic Analysis of BTK Inhibition in Patients with Chronic Lymphocytic Leukemia Treated with Acalabrutinib
Fig S5 from Pharmacodynamic Analysis of BTK Inhibition in Patients with Chronic Lymphocytic Leukemia Treated with Acalabrutinib Open
Rate of change in percent free BTK per day.
View article: Fig S3 from Pharmacodynamic Analysis of BTK Inhibition in Patients with Chronic Lymphocytic Leukemia Treated with Acalabrutinib
Fig S3 from Pharmacodynamic Analysis of BTK Inhibition in Patients with Chronic Lymphocytic Leukemia Treated with Acalabrutinib Open
Flow cytometry gating strategy for pBTK after in vitro stimulation.
View article: Table S2 from Pharmacodynamic Analysis of BTK Inhibition in Patients with Chronic Lymphocytic Leukemia Treated with Acalabrutinib
Table S2 from Pharmacodynamic Analysis of BTK Inhibition in Patients with Chronic Lymphocytic Leukemia Treated with Acalabrutinib Open
Supplementary Table S2: Assay IDs for genes analyzed by RT-PCR
View article: Table S1 from Pharmacodynamic Analysis of BTK Inhibition in Patients with Chronic Lymphocytic Leukemia Treated with Acalabrutinib
Table S1 from Pharmacodynamic Analysis of BTK Inhibition in Patients with Chronic Lymphocytic Leukemia Treated with Acalabrutinib Open
Supplementary Table S1: Patient characteristics
View article: Fig S4 from Pharmacodynamic Analysis of BTK Inhibition in Patients with Chronic Lymphocytic Leukemia Treated with Acalabrutinib
Fig S4 from Pharmacodynamic Analysis of BTK Inhibition in Patients with Chronic Lymphocytic Leukemia Treated with Acalabrutinib Open
Flow cytometry gating strategy for CD69 after in vitro stimulation.
View article: Data from Pharmacodynamic Analysis of BTK Inhibition in Patients with Chronic Lymphocytic Leukemia Treated with Acalabrutinib
Data from Pharmacodynamic Analysis of BTK Inhibition in Patients with Chronic Lymphocytic Leukemia Treated with Acalabrutinib Open
Purpose:To determine the pharmacodynamic relationship between target occupancy of Bruton tyrosine kinase (BTK) and inhibition of downstream signaling.Patients and Methods:Patients with chronic lymphocytic leukemia (CLL) enrolled in a phase…
View article: Table S3 from Pharmacodynamic Analysis of BTK Inhibition in Patients with Chronic Lymphocytic Leukemia Treated with Acalabrutinib
Table S3 from Pharmacodynamic Analysis of BTK Inhibition in Patients with Chronic Lymphocytic Leukemia Treated with Acalabrutinib Open
Supplementary Table S3: List of patients included in the analysis of rebound in cellular signaling during drug withholding
View article: Fig S1 from Pharmacodynamic Analysis of BTK Inhibition in Patients with Chronic Lymphocytic Leukemia Treated with Acalabrutinib
Fig S1 from Pharmacodynamic Analysis of BTK Inhibition in Patients with Chronic Lymphocytic Leukemia Treated with Acalabrutinib Open
Flow cytometry gating strategy for intracellular phosphor-proteins assessed ex-vivo.
View article: Table S1 from Pharmacodynamic Analysis of BTK Inhibition in Patients with Chronic Lymphocytic Leukemia Treated with Acalabrutinib
Table S1 from Pharmacodynamic Analysis of BTK Inhibition in Patients with Chronic Lymphocytic Leukemia Treated with Acalabrutinib Open
Supplementary Table S1: Patient characteristics
View article: Fig S1 from Pharmacodynamic Analysis of BTK Inhibition in Patients with Chronic Lymphocytic Leukemia Treated with Acalabrutinib
Fig S1 from Pharmacodynamic Analysis of BTK Inhibition in Patients with Chronic Lymphocytic Leukemia Treated with Acalabrutinib Open
Flow cytometry gating strategy for intracellular phosphor-proteins assessed ex-vivo.
View article: Figure S1 from Enitociclib, a Selective CDK9 Inhibitor, Induces Complete Regression of MYC+ Lymphoma by Downregulation of RNA Polymerase II Mediated Transcription
Figure S1 from Enitociclib, a Selective CDK9 Inhibitor, Induces Complete Regression of MYC+ Lymphoma by Downregulation of RNA Polymerase II Mediated Transcription Open
Supplementary Figure 1 shows the principal component analysis of RNA sequencing of either SU-DHL-4 and SU-DHL-10 cell lines as well as that from RNA sequencing of patient blood samples.
View article: FIGURE 5 from Enitociclib, a Selective CDK9 Inhibitor, Induces Complete Regression of MYC+ Lymphoma by Downregulation of RNA Polymerase II Mediated Transcription
FIGURE 5 from Enitociclib, a Selective CDK9 Inhibitor, Induces Complete Regression of MYC+ Lymphoma by Downregulation of RNA Polymerase II Mediated Transcription Open
Comparison of DEGs identified in MYC+ DLBCL cell lines to blood samples from enitociclib-treated patienst with MYC+ NHL. A, Comparison of significant DEGs (Padj ≤ 0.05, fold change ≥2) after at 4 hours pretreatment…
View article: FIGURE 4 from Enitociclib, a Selective CDK9 Inhibitor, Induces Complete Regression of MYC+ Lymphoma by Downregulation of RNA Polymerase II Mediated Transcription
FIGURE 4 from Enitociclib, a Selective CDK9 Inhibitor, Induces Complete Regression of MYC+ Lymphoma by Downregulation of RNA Polymerase II Mediated Transcription Open
Enitociclib treatment confers a robust shift in transcriptional activity in MYC+ DLBCL cell lines. A, Comparison of significant DEGs (Padj ≤ 0.05, fold change ≥2) after 4 hours pretreatment of DLBLC cell lin…
View article: TABLE 1 from Enitociclib, a Selective CDK9 Inhibitor, Induces Complete Regression of MYC+ Lymphoma by Downregulation of RNA Polymerase II Mediated Transcription
TABLE 1 from Enitociclib, a Selective CDK9 Inhibitor, Induces Complete Regression of MYC+ Lymphoma by Downregulation of RNA Polymerase II Mediated Transcription Open
Response and pharmacokinetics properties of patients with DH-DLBCL and other patients with MYC+ NHL (n = 15) treated with 30 mg enitociclib i.v. once weekly
View article: Table S2 from Enitociclib, a Selective CDK9 Inhibitor, Induces Complete Regression of MYC+ Lymphoma by Downregulation of RNA Polymerase II Mediated Transcription
Table S2 from Enitociclib, a Selective CDK9 Inhibitor, Induces Complete Regression of MYC+ Lymphoma by Downregulation of RNA Polymerase II Mediated Transcription Open
Supplementary Table 2 contains the statistical analysis for pSer2 downregulation in SU-DHL-4 and SU-DHL-10 cell lines across CDK9 inhibitor treatments.
View article: Figure S1 from Enitociclib, a Selective CDK9 Inhibitor, Induces Complete Regression of MYC+ Lymphoma by Downregulation of RNA Polymerase II Mediated Transcription
Figure S1 from Enitociclib, a Selective CDK9 Inhibitor, Induces Complete Regression of MYC+ Lymphoma by Downregulation of RNA Polymerase II Mediated Transcription Open
Supplementary Figure 1 shows the principal component analysis of RNA sequencing of either SU-DHL-4 and SU-DHL-10 cell lines as well as that from RNA sequencing of patient blood samples.
View article: Figure S2 from Enitociclib, a Selective CDK9 Inhibitor, Induces Complete Regression of MYC+ Lymphoma by Downregulation of RNA Polymerase II Mediated Transcription
Figure S2 from Enitociclib, a Selective CDK9 Inhibitor, Induces Complete Regression of MYC+ Lymphoma by Downregulation of RNA Polymerase II Mediated Transcription Open
Supplementary Figure 2: Downregulation of MYC and MCL1 is detected in the whole blood of Enitociclib-treated DH-DLBCL as well as other MYC+ NHL patients
View article: Table S3 from Enitociclib, a Selective CDK9 Inhibitor, Induces Complete Regression of MYC+ Lymphoma by Downregulation of RNA Polymerase II Mediated Transcription
Table S3 from Enitociclib, a Selective CDK9 Inhibitor, Induces Complete Regression of MYC+ Lymphoma by Downregulation of RNA Polymerase II Mediated Transcription Open
Supplementary Table 3 contains the top DEGS from an unbiased analysis of RNAseq from MYC+ DLBCL cell lines treated with CDK9 inhibitors.
View article: FIGURE 4 from Enitociclib, a Selective CDK9 Inhibitor, Induces Complete Regression of MYC+ Lymphoma by Downregulation of RNA Polymerase II Mediated Transcription
FIGURE 4 from Enitociclib, a Selective CDK9 Inhibitor, Induces Complete Regression of MYC+ Lymphoma by Downregulation of RNA Polymerase II Mediated Transcription Open
Enitociclib treatment confers a robust shift in transcriptional activity in MYC+ DLBCL cell lines. A, Comparison of significant DEGs (Padj ≤ 0.05, fold change ≥2) after 4 hours pretreatment of DLBLC cell lin…
View article: FIGURE 1 from Enitociclib, a Selective CDK9 Inhibitor, Induces Complete Regression of MYC+ Lymphoma by Downregulation of RNA Polymerase II Mediated Transcription
FIGURE 1 from Enitociclib, a Selective CDK9 Inhibitor, Induces Complete Regression of MYC+ Lymphoma by Downregulation of RNA Polymerase II Mediated Transcription Open
Enitociclib delivers robust inhibition of RNA polymerase II Ser2 phosphorylation for up to 48 hours in cell lines. A, The gene expression of MYC, and MCL1 as determined by RNA-seq expressed as transcripts per million (…