The discovery study reported an A2780 thymidine-uptake growth-inhibition IC50 of 0.004 μM for compound 13 (SCH 727965), relative to vehicle controls. [3]
Across the 23-line pediatric panel, 96 h exposure gave a median absolute IC50 of 7.5 nM (range 3.4–11.2 nM). Most lines showed a cytotoxic response pattern, but selected neuroblastoma lines showed increased survival at high concentrations relative to their response minima. [4]
CDK1 enzyme assay using dinaciclib as a reference inhibitor
Biochemical assay · CDK1 protein with histone H1 substrate; ADP-Glo luminescence assay [1]
The authors described complete CDK1 inhibition by dinaciclib at the three tested reference-compound concentrations. This fixed-concentration result does not establish a dinaciclib IC50 or CDK subtype selectivity.
Literature-Reported Treatment Conditions
- Treatment concentration
- 1, 10 and 100 μM
- Exposure duration
- 60 min kinase reaction
- Method
- Cell-free CDK1 kinase assay
- Co-treatment
- None
- Reported limits
- Dinaciclib salt, explicit stereochemical characterization, lot and replicate count are not given in the read main-text assay description. Table S8 not retrieved.
Methods and source locations
Compound reported in the paper: Dinaciclib (SCH 727965)
Compound-level research evidence; tested supplier/form and model conditions apply. No Adooq lot validation or clinical efficacy inference.
Sections 2.10 (Kinase Assay) and 3.7 (Kinase Assay results)
CDK1 activity relative to enzyme control: ADP-Glo assay; 1 ng CDK1, histone H1 0.2 μg/μL, ATP 50 μM; enzyme control without compound and no-enzyme control; RO-3306 reference comparator. — Sections 2.10 (Kinase Assay) and 3.7 (Kinase Assay results)
A2780 growth inhibition by compound 13
Cell-based study · A2780 human ovarian carcinoma cells [3]
Table 2 reports an in-cell IC50 of 0.004 μM for compound 13, identified as SCH 727965. The endpoint is thymidine uptake growth inhibition relative to vehicle controls.
Literature-Reported Treatment Conditions
- Treatment concentration
- Dose-response assay; tested concentration range not specified in the read main text
- Method
- Thymidine uptake growth inhibition
- Vehicle
- Vehicle controls; composition not specified in the read main text
- Co-treatment
- None
- Reported limits
- Exposure duration, cell assay replication and vehicle composition not stated in the read main text; cited earlier assay methods were not acquired.
Methods and source locations
Compound reported in the paper: Dinaciclib (SCH 727965); Compound label in the paper: Compound 13
Compound-level research evidence; tested supplier/form and model conditions apply. No Adooq lot validation or clinical efficacy inference.
Table 2, compound 13, In-Cell IC50 column and footnote b; concluding paragraph identifying compound 13 as SCH 727965
A2780 thymidine uptake growth inhibition: Thymidine uptake assay; inhibition calculated relative to vehicle controls and plotted on log-linear plots to derive IC50 (Table 2 footnote b). — Table 2, compound 13, In-Cell IC50 column and footnote b; concluding paragraph identifying compound 13 as SCH 727965
Pediatric cell-line viability panel and nonmonotonic responses
Cell-based study · PPTP panel of 23 pediatric cancer cell lines [4]
After 96 h, the panel median absolute IC50 was 7.5 nM (range 3.4–11.2 nM). Most lines showed a cytotoxic activity pattern. Selected neuroblastoma lines had higher survival at high concentrations than near the minimum of their response curves.
Literature-Reported Treatment Conditions
- Treatment concentration
- 0.1 nM to 1 μM
- Exposure duration
- 96 h
- Method
- DIMSCAN viable-cell assay
- Co-treatment
- None
- Reported limits
- In vitro vehicle composition and replicate numbers are not specified in the acquired main-text description.
Methods and source locations
Compound reported in the paper: Dinaciclib (SCH 727965)
Compound-level research evidence; tested supplier/form and model conditions apply. No Adooq lot validation or clinical efficacy inference.
Materials and Methods: In vitro testing; Results: In vitro testing; Table I; Figure 1B and caption
Cell survival reduced to 50% of control (absolute IC50): DIMSCAN fluorescence-based viable-cell quantification after 96 h. These are absolute IC50 values, not the separate relative IC50 column. — Table I; Methods: In vitro testing
Higher T/C% at 1 μM than at 30 nM in NB-EBc1 and CHLA-136: DIMSCAN; qualitative curve direction verified in original Figure 1B. No survival percentages estimated from curves. — Figure 1B and caption; Results: In vitro testing
Neuroblastoma phosphorylation responses consistent with CDK2/CDK9 inhibition
Cell-based study · NGP, SH-SY5Y and SK-N-AS human neuroblastoma cells [2]
Dinaciclib reduced Rb Ser807/811 and RNA polymerase II Ser2 phosphorylation in time- and concentration-dependent experiments. These cellular substrate readouts support pathway inhibition but do not independently establish exclusive CDK2/CDK9 causation.
Literature-Reported Treatment Conditions
- Treatment concentration
- Time course: 0.2 μM; 4 h concentration series: 0, 0.1, 0.2, 0.5 and 1 μM
- Exposure duration
- Time course: 0, 2, 4, 6 and 8 h; concentration series: 4 h
- Method
- Immunoblotting
- Co-treatment
- None
- Reported limits
- Specific solvent matching for Figure 3c,d and independent replicate count are not specified in the read caption/methods.
Methods and source locations
Compound reported in the paper: Dinaciclib (SCH 727965)
Compound-level research evidence; tested supplier/form and model conditions apply. No Adooq lot validation or clinical efficacy inference.
Results: Dinaciclib abrogates CDK2 and CDK9 activity; Figure 3c,d and caption; Methods: Reagents, Cell Culture, Immunoblotting
Rb Ser807/811 and RNA polymerase II Ser2 phosphorylation: Immunoblots with total Rb and total RNA polymerase II comparators and β-actin loading control; zero-time/zero-dose controls shown. No fold change or IC50 calculated. — Figure 3c,d; corresponding Results and caption
