Sapitinib showed model-dependent cellular activity in a seven-line chordoma panel. Reported geometric-mean EC50 values ranged from 0.015–0.054 µM in four responsive lines, while U-CH2, U-CH10 and JHC7 had values of 8.565–26.132 µM. [1]
In SUM149 and FC-IBC-02 inflammatory breast cancer cells, 1 µM AZD8931 increased Annexin V-positive cells after 48 and 72 h compared with controls (P < 0.001; three independent experiments). [2]
EGFR phosphorylation response in chordoma cells
Cell-based study · U-CH1 and UM-Chor1 chordoma cells (immunoblot); chordoma panel and NCI-N87 (ELISA) [1]
Sapitinib suppressed EGFR phosphorylation in cellular assays. These are receptor-signaling endpoints, not isolated-kinase IC50 values.
Literature-Reported Treatment Conditions
- Treatment concentration
- Figure 3A sapitinib series: 0.12, 0.37, 1.1, 3.3 and 10 µM; Figure 3B uses concentration-response assays.
- Exposure duration
- 4 h inhibitor treatment followed by 15 min EGF stimulation; overnight serum starvation.
- Method
- EGF stimulation at 50 ng/mL; phospho-EGFR measured by western blot and ELISA.
- Vehicle
- 2.5% DMSO in the serum-starved, EGF-stimulated vehicle control (Figure 3 caption).
- Reported limits
- No numeric ELISA EC50 is extracted from graph bars. The separate supplementary antibody/method files were not acquired; qualitative receptor suppression is restricted to the published main figure and described controls.
Methods and source locations
Compound reported in the paper: Sapitinib (AZD8931)
Compound-level evidence for AZD8931; the tested material was not an Adooq lot. No salt conversion or product-lot validation is implied.
Figure 3A–B; Results: EGFR/ERBB family inhibitors suppressed p-EGFR; Materials and methods: Protein kinase inhibitors, ELISA
EGFR phosphorylation after EGF stimulation: ELISA and western blot; endogenous, untreated serum-starved and DMSO vehicle controls described in Figure 3 caption. — Figure 3A–B and caption; Results: EGFR/ERBB family inhibitors suppressed p-EGFR
Model-dependent cellular potency in a chordoma panel
Cell-based study · Seven chordoma lines; normal adult human dermal fibroblasts (NAHDF) and NCI-N87 gastric cancer controls [1]
Sapitinib cellular EC50 values varied widely across models. Four chordoma lines had submicromolar values; U-CH2, U-CH10 and JHC7 were less sensitive.
Literature-Reported Treatment Conditions
- Method
- Phenotypic cell-response concentration series; main screening workflow uses WST1 and hit confirmation uses a 10-point dose-response format with staurosporine as a positive assay control.
- Reported limits
- The commercial validation panel Table 3 does not separately give its treatment duration, vehicle or full dosing series in the acquired main text. The general single-point screen used 96 h, but that duration is not assigned to Table 3 as a separately verified condition. Supplementary methods were not acquired.
Methods and source locations
Compound reported in the paper: Sapitinib (AZD8931)
Compound-level evidence for AZD8931; the tested material was not an Adooq lot. No salt conversion or product-lot validation is implied.
Table 3; Results: Commercially available EGFR/ERBB family inhibitors; Methods: Cells and cell lines, Hit confirmation
Sapitinib cell-response potency by model: Table 3 phenotypic response; EC50 is not a biochemical IC50. The hit-confirmation methods describe three independent experiments with two replicates/experiment; Table 3 does not separately restate n. — Table 3, Sapitinib row and EC50 header/footnote
Sapitinib maximum cell-response inhibition at the highest tested concentration: Reported Table 3 maximum percentage inhibition; preserve the normalized 103% value as printed. Highest concentration specific to this commercial panel is not separately verified. — Table 3, Sapitinib row and maximum percentage inhibition header
Annexin V response in inflammatory breast cancer cells
Cell-based study · SUM149 and FC-IBC-02 human inflammatory breast cancer cells [2]
AZD8931 increased Annexin V-positive cells compared with controls in both models at 48 and 72 h.
Literature-Reported Treatment Conditions
- Treatment concentration
- 1 µM
- Exposure duration
- 48 or 72 h
- Method
- Annexin V-PE and 7-AAD staining, Guava Nexin assay/Guava flow cytometry.
- Reported limits
- Chemical identity of the cellular vehicle and lot-specific analytical characterization are not specified in the acquired methods. A control group is shown in Figure 3C–D.
Methods and source locations
Compound reported in the paper: AZD8931
Compound-level evidence for AZD8931; the tested material was not an Adooq lot. No salt conversion or product-lot validation is implied.
Figure 3C–D; Results: AZD8931 inhibits proliferation and induces apoptosis; Methods: Cell proliferation and apoptotic assay
Annexin V-positive cells versus control: Guava Nexin assay; percentages not inferred from bar heights. — Figure 3C–D, caption and corresponding Results paragraph
