Vivek C. Abraham
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View article: Supplementary Table 4 from PARP1 Trapping by PARP Inhibitors Drives Cytotoxicity in Both Cancer Cells and Healthy Bone Marrow
Supplementary Table 4 from PARP1 Trapping by PARP Inhibitors Drives Cytotoxicity in Both Cancer Cells and Healthy Bone Marrow Open
Bone Marrow IC50s broken into cell type.
View article: Wilsbacher et. al. supplement from Discovery and Characterization of Novel Nonsubstrate and Substrate NAMPT Inhibitors
Wilsbacher et. al. supplement from Discovery and Characterization of Novel Nonsubstrate and Substrate NAMPT Inhibitors Open
Supplementary methods, tables S1-S3, and supplementary figures 1-7
View article: Supplementary Figure 1 from PARP1 Trapping by PARP Inhibitors Drives Cytotoxicity in Both Cancer Cells and Healthy Bone Marrow
Supplementary Figure 1 from PARP1 Trapping by PARP Inhibitors Drives Cytotoxicity in Both Cancer Cells and Healthy Bone Marrow Open
Association of PARP1 and H2A.X detected by Proximity Ligation Assay (PLA).
View article: Supplementary Table 4 from PARP1 Trapping by PARP Inhibitors Drives Cytotoxicity in Both Cancer Cells and Healthy Bone Marrow
Supplementary Table 4 from PARP1 Trapping by PARP Inhibitors Drives Cytotoxicity in Both Cancer Cells and Healthy Bone Marrow Open
Bone Marrow IC50s broken into cell type.
View article: Supplementary Figure 2 from PARP1 Trapping by PARP Inhibitors Drives Cytotoxicity in Both Cancer Cells and Healthy Bone Marrow
Supplementary Figure 2 from PARP1 Trapping by PARP Inhibitors Drives Cytotoxicity in Both Cancer Cells and Healthy Bone Marrow Open
Association of PARP1 and other histone proteins detected by Proximity Ligation Assay (PLA).
View article: Supplementary Table 3 from PARP1 Trapping by PARP Inhibitors Drives Cytotoxicity in Both Cancer Cells and Healthy Bone Marrow
Supplementary Table 3 from PARP1 Trapping by PARP Inhibitors Drives Cytotoxicity in Both Cancer Cells and Healthy Bone Marrow Open
IC50 values of PARPi vs BM-CFU and BM-PAR
View article: Data from PARP1 Trapping by PARP Inhibitors Drives Cytotoxicity in Both Cancer Cells and Healthy Bone Marrow
Data from PARP1 Trapping by PARP Inhibitors Drives Cytotoxicity in Both Cancer Cells and Healthy Bone Marrow Open
PARP inhibitors have recently been approved as monotherapies for the treatment of recurrent ovarian cancer and metastatic BRCA-associated breast cancer, and ongoing studies are exploring additional indications and combinations with …
View article: Supplementary Figure 1 from PARP1 Trapping by PARP Inhibitors Drives Cytotoxicity in Both Cancer Cells and Healthy Bone Marrow
Supplementary Figure 1 from PARP1 Trapping by PARP Inhibitors Drives Cytotoxicity in Both Cancer Cells and Healthy Bone Marrow Open
Association of PARP1 and H2A.X detected by Proximity Ligation Assay (PLA).
View article: Supplementary Table 1 from PARP1 Trapping by PARP Inhibitors Drives Cytotoxicity in Both Cancer Cells and Healthy Bone Marrow
Supplementary Table 1 from PARP1 Trapping by PARP Inhibitors Drives Cytotoxicity in Both Cancer Cells and Healthy Bone Marrow Open
IC50s (nM) for inhibition of enzyme activity for PARP family members
View article: Wilsbacher et. al. supplement from Discovery and Characterization of Novel Nonsubstrate and Substrate NAMPT Inhibitors
Wilsbacher et. al. supplement from Discovery and Characterization of Novel Nonsubstrate and Substrate NAMPT Inhibitors Open
Supplementary methods, tables S1-S3, and supplementary figures 1-7
View article: Supplementary Table 2 from PARP1 Trapping by PARP Inhibitors Drives Cytotoxicity in Both Cancer Cells and Healthy Bone Marrow
Supplementary Table 2 from PARP1 Trapping by PARP Inhibitors Drives Cytotoxicity in Both Cancer Cells and Healthy Bone Marrow Open
Clinical RP2D concentrations for PARP inhibitors.
View article: Data from Discovery and Characterization of Novel Nonsubstrate and Substrate NAMPT Inhibitors
Data from Discovery and Characterization of Novel Nonsubstrate and Substrate NAMPT Inhibitors Open
Cancer cells are highly reliant on NAD+-dependent processes, including glucose metabolism, calcium signaling, DNA repair, and regulation of gene expression. Nicotinamide phosphoribosyltransferase (NAMPT), the rate-limiting enzym…
View article: Data from PARP1 Trapping by PARP Inhibitors Drives Cytotoxicity in Both Cancer Cells and Healthy Bone Marrow
Data from PARP1 Trapping by PARP Inhibitors Drives Cytotoxicity in Both Cancer Cells and Healthy Bone Marrow Open
PARP inhibitors have recently been approved as monotherapies for the treatment of recurrent ovarian cancer and metastatic BRCA-associated breast cancer, and ongoing studies are exploring additional indications and combinations with …
View article: Supplementary Table 2 from PARP1 Trapping by PARP Inhibitors Drives Cytotoxicity in Both Cancer Cells and Healthy Bone Marrow
Supplementary Table 2 from PARP1 Trapping by PARP Inhibitors Drives Cytotoxicity in Both Cancer Cells and Healthy Bone Marrow Open
Clinical RP2D concentrations for PARP inhibitors.
View article: Data from Discovery and Characterization of Novel Nonsubstrate and Substrate NAMPT Inhibitors
Data from Discovery and Characterization of Novel Nonsubstrate and Substrate NAMPT Inhibitors Open
Cancer cells are highly reliant on NAD+-dependent processes, including glucose metabolism, calcium signaling, DNA repair, and regulation of gene expression. Nicotinamide phosphoribosyltransferase (NAMPT), the rate-limiting enzym…
View article: Supplementary Table 1 from PARP1 Trapping by PARP Inhibitors Drives Cytotoxicity in Both Cancer Cells and Healthy Bone Marrow
Supplementary Table 1 from PARP1 Trapping by PARP Inhibitors Drives Cytotoxicity in Both Cancer Cells and Healthy Bone Marrow Open
IC50s (nM) for inhibition of enzyme activity for PARP family members
View article: Supplementary Figure 2 from PARP1 Trapping by PARP Inhibitors Drives Cytotoxicity in Both Cancer Cells and Healthy Bone Marrow
Supplementary Figure 2 from PARP1 Trapping by PARP Inhibitors Drives Cytotoxicity in Both Cancer Cells and Healthy Bone Marrow Open
Association of PARP1 and other histone proteins detected by Proximity Ligation Assay (PLA).
View article: Supplementary Table 3 from PARP1 Trapping by PARP Inhibitors Drives Cytotoxicity in Both Cancer Cells and Healthy Bone Marrow
Supplementary Table 3 from PARP1 Trapping by PARP Inhibitors Drives Cytotoxicity in Both Cancer Cells and Healthy Bone Marrow Open
IC50 values of PARPi vs BM-CFU and BM-PAR
View article: Supplementary Data from Hexavalent TRAIL Fusion Protein Eftozanermin Alfa Optimally Clusters Apoptosis-Inducing TRAIL Receptors to Induce On-Target Antitumor Activity in Solid Tumors
Supplementary Data from Hexavalent TRAIL Fusion Protein Eftozanermin Alfa Optimally Clusters Apoptosis-Inducing TRAIL Receptors to Induce On-Target Antitumor Activity in Solid Tumors Open
Supplementary file containing all supplementary figures and tables
View article: Data from Hexavalent TRAIL Fusion Protein Eftozanermin Alfa Optimally Clusters Apoptosis-Inducing TRAIL Receptors to Induce On-Target Antitumor Activity in Solid Tumors
Data from Hexavalent TRAIL Fusion Protein Eftozanermin Alfa Optimally Clusters Apoptosis-Inducing TRAIL Receptors to Induce On-Target Antitumor Activity in Solid Tumors Open
TRAIL can activate cell surface death receptors, resulting in potent tumor cell death via induction of the extrinsic apoptosis pathway. Eftozanermin alfa (ABBV-621) is a second generation TRAIL receptor agonist engineered as an IgG1-Fc mut…
View article: Supplementary Data from Hexavalent TRAIL Fusion Protein Eftozanermin Alfa Optimally Clusters Apoptosis-Inducing TRAIL Receptors to Induce On-Target Antitumor Activity in Solid Tumors
Supplementary Data from Hexavalent TRAIL Fusion Protein Eftozanermin Alfa Optimally Clusters Apoptosis-Inducing TRAIL Receptors to Induce On-Target Antitumor Activity in Solid Tumors Open
Supplementary file containing all supplementary figures and tables
View article: Data from Hexavalent TRAIL Fusion Protein Eftozanermin Alfa Optimally Clusters Apoptosis-Inducing TRAIL Receptors to Induce On-Target Antitumor Activity in Solid Tumors
Data from Hexavalent TRAIL Fusion Protein Eftozanermin Alfa Optimally Clusters Apoptosis-Inducing TRAIL Receptors to Induce On-Target Antitumor Activity in Solid Tumors Open
TRAIL can activate cell surface death receptors, resulting in potent tumor cell death via induction of the extrinsic apoptosis pathway. Eftozanermin alfa (ABBV-621) is a second generation TRAIL receptor agonist engineered as an IgG1-Fc mut…