In a six-day growth-inhibition screen, BX-795 produced higher dose-response AUC bars in endometrial cancer organoids REME9 and REME16 than in conventional AN3 CA and RL95-2 cells, consistent with weaker inhibition in the organoids across the screen. This was a qualitative model comparison, without a BX-795-specific significance test. [3]
Direct inhibition of TBK1 and IKKε peptide phosphorylation
Biochemical assay · Purified GST-TBK1 or GST-IKKε; TBK1-Tide peptide substrate [1]
Increasing BX-795 concentrations reduced peptide phosphorylation by both enzymes relative to the zero-inhibitor control. These are cell-free activity measurements, not cellular potency values.
Literature-Reported Treatment Conditions
- Treatment concentration
- 0, 10, 100, 250, 500 and 10000 nM (Figure 3 labels)
- Exposure duration
- 20 min pretreatment at room temperature; kinase reaction 30 min at 30°C (Figure 3 caption)
- Method
- In vitro kinase assay using purified GST-tagged enzymes and TBK1-Tide.
- Reported limits
- BX-795 supplier/form details and replicate number are not specified in the Figure 3 caption or the relevant reagent/method paragraphs. General kinase methods describe a 1 h incubation; the adopted experiment uses its explicit 30 min caption.
Methods and source locations
Compound reported in the paper: BX-795; Compound label in the paper: BX-795 (BX795)
Applies to the named research compound in the reported model; no current Adooq SKU, lot, salt equivalence or clinical efficacy validation.
Figure 3A-B/caption; Results assay-validation paragraph; Materials and Methods, Plasmids/Peptides and In vitro Kinase Assays
TBK1- or IKKε-catalyzed peptide phosphorylation: Radiolabeled phosphate incorporation; 50 µM peptide and 100 µM ATP; zero-inhibitor activity set to 100%. — Figure 3A-B/caption
BX-795 response in endometrial cancer organoids and cell lines
Cell-based study · Endometrial cancer organoids REME9 and REME16; conventional cell lines AN3 CA and RL95-2 [3]
The BX-795 AUC bars were higher in REME9 and REME16 than in AN3 CA and RL95-2, consistent with weaker inhibition in the organoids over the plotted screen. This qualitative comparison has no reported BX-795-specific significance test.
Literature-Reported Treatment Conditions
- Treatment concentration
- Concentration series up to 20 µM; precise lower bound unresolved between methods and Figure 6 caption.
- Exposure duration
- 144 h after compound addition; compound added 24 h after seeding.
- Method
- 384-well growth-inhibition screen; ATP-based viability normalized to vehicle.
- Vehicle
- DMSO; maximum 0.1% stated in the shared growth-inhibition methods.
- Reported limits
- Methods give ten serial concentrations from 1.0 nM to 20 µM; Figure 6 caption gives 0.1–20 µM. Neither range is silently substituted for the other. Exact BX-795 AUC values, AUC units and a BX-795-specific statistical comparison are not supplied in Figure 6.
Methods and source locations
Compound reported in the paper: BX-795; Compound label in the paper: BX-795 (BX795)
Applies to the named research compound in the reported model; no current Adooq SKU, lot, salt equivalence or clinical efficacy validation.
Table II, BX-795 row; Figure 6/caption; growth inhibition assay methods; Results, anticancer-agent evaluation
Integrated growth-inhibition response: Six-day ATP-based CellTiter-Glo 3D viability assay in the 384-well screen; viability normalized to vehicle control. No exact AUC values estimated from bars. — Figure 6, BX-795 row across four model panels/caption
PDK1-null control limits interpretation of BX-795-induced G2/M arrest
Cell-based study · Murine PDK1+/+ and PDK1−/− embryonic stem cells [2]
BX-795 increased the G2/M population in both wild-type and PDK1-null cells relative to DMSO. Persistence in knockout cells shows that this phenotype cannot be attributed solely to PDK1 inhibition in this model.
Literature-Reported Treatment Conditions
- Treatment concentration
- 5 µM BX-795
- Exposure duration
- 48 h; medium with inhibitor or DMSO replaced after 24 h.
- Method
- Cell-cycle analysis in ES cells cultured with 15% serum replacement and LIF.
- Vehicle
- DMSO control
- Reported limits
- Vehicle percentage and source/lot for BX-795 are not specified in the adopted experiment description. Positive control: nocodazole 100 ng/ml, added 24 h before harvest.
Methods and source locations
Compound reported in the paper: BX-795; Compound label in the paper: BX-795 (BX795)
Applies to the named research compound in the reported model; no current Adooq SKU, lot, salt equivalence or clinical efficacy validation.
Figure 1B/caption; Results, The effect of BX-795 on G2/M arrest is mostly PDK1 independent; Cell culture and Cell cycle analysis methods
Cell-cycle distribution: Propidium iodide staining and flow cytometry; DMSO negative control; nocodazole positive control. No exact fractions inferred from stacked bars. — Figure 1B/caption and immediately following Results paragraph
