PF 431396 decreased cell adhesion in MV4-11 parental cells in a dose-dependent manner compared with untreated cells. In A375 melanoma cells, PF 431396 treatment under dual FAK/Pyk2 inhibition did not modify invadopodia activity compared with control conditions. In RAW 264.7 macrophages, post-phagocytosis treatment with PF 431396 significantly decreased the proportion of cells with a high bacterial burden compared with untreated cells. In MV4-11R cells compared with mock-treated MV4-11R cells, PF 431396 treatment resulted, in the majority of cases, in complete compensation of the effects on protein translation observed in resistant compared with parental cells. [1,2,3]
Literature-reported observations and conditions; not Adooq-tested protocols or general treatment recommendations.
Dose-dependent decrease in cell adhesion
Cell-based study · MV4-11 parental cells [1]
MV4-11 parental cells received the study compound before the assay, with untreated cells as the control. Treatment decreased cell adhesion in a dose-dependent manner.
Literature-Reported Treatment Conditions
- Exposure duration
- 24 h prior to the assay
- Reported limits
- Not stated in the sentences used: dose, route, vehicle.
Methods and source locations
Compound reported in the paper: PF 431396
Literature evidence for the named compound in the stated model; no Adooq product-use or lot-performance claim.
Results > PTK2B/FAK inhibitor PF-431396 abolishes enhanced cell migration in midostaurin-resistant cells (S102); Fig. 3 legend (S200, S201)
cell adhesion: cell adhesion; comparator: Untreated cells — Results > PTK2B/FAK inhibitor PF-431396 abolishes enhanced cell migration in midostaurin-resistant cells (S102)
Invadopodia Activity in Melanoma Cells Following Treatment
Cell-based study · A375 melanoma cells lines [2]
In melanoma cell lines, treatment with the tested compound did not modify invadopodia activity compared with control conditions, as assessed by mean area of degradation.
Literature-Reported Treatment Conditions
- Treatment concentration
- 1 µM
- Exposure duration
- 24 h
- Reported limits
- Not stated in the sentences used: route, vehicle.
Methods and source locations
Compound reported in the paper: PF 431396
Literature evidence for the named compound in the stated model; no Adooq product-use or lot-performance claim.
Materials and methods > Matrix degradation assay and immunofluorescence (S15, S17); Results > The dual FAK/Pyk2 inhibitor PF-431396 reduced both migration and matrix degradation of melanoma cells (S173, S174); Fig. 8 legend (S245, S248)
mean area of degradation: mean area of degradation; comparator: control conditions — Results > The dual FAK/Pyk2 inhibitor PF-431396 reduced both migration and matrix degradation of melanoma cells (S174); Fig. 8 legend (S248)
Treatment Reduced the Proportion of Macrophages With High Bacterial Burden
Cell-based study · RAW 264.7 macrophages [3]
In RAW 264.7 macrophages, the compound was added at 10 µM post-phagocytosis. Compared with untreated cells, treatment significantly decreased the proportion of cells with a high bacterial burden, reported as 9.01 % at 6 h p.i. and 6.87 % at 12 h p.i.
Literature-Reported Treatment Conditions
- Treatment concentration
- 10 µM
- Exposure duration
- post-phagocytosis; 6 h p.i.; 12 h p.i.
- Method
- added
- Co-treatment
- Other interventions in this design: LF82::rpsMGFP m.o.i. of 100; lipopolysaccharide 1 µg ml−1; gentamicin 50 µg ml−1. Compound effect isolated by the comparison: Untreated cells.
- Reported limits
- Not stated in the sentences used: vehicle.
Methods and source locations
Compound reported in the paper: PF 431396
Evidence for PF 431396 as the hydrate form reported in the paper, not the free base/neutral form supplied as A11142; no salt equivalence, dose conversion or lot validation.
Methods > Gentamicin protection assay for AIEC infection (S9, S10, S11); Results > PF-431396 hydrate blocks intracellular LF82 replication without affecting overall numbers of infected cells (S97, S100, S101, S103, S104); Fig. 4. legend (S149, S151)
percentage of the total population: percentage of the total population; comparator: Untreated cells — Results > PF-431396 hydrate blocks intracellular LF82 replication without affecting overall numbers of infected cells (S97, S103)
Compensation of protein translation changes in resistant cells
Cell-based study · MV4-11R cells [1]
MV4-11R cells were exposed to PF 431396 at 300 nM for 16 h and compared with mock-treated MV4-11R cells. Nascent proteomics showed that treatment resulted, in the majority of cases, in complete compensation of the effects on protein translation observed in resistant compared with parental cells.
Literature-Reported Treatment Conditions
- Treatment concentration
- 300 nM
- Exposure duration
- 16 h
- Method
- exposed
- Co-treatment
- Other interventions in this design: PKC-412/midostaurin. Compound effect isolated by the comparison: MV4-11R treated with 300 nM PF-431396 compared to MV4-11R cells with mock treatment (R).
- Reported limits
- Not stated in the sentences used: vehicle.
Methods and source locations
Compound reported in the paper: PF 431396
Literature evidence for the named compound in the stated model; no Adooq product-use or lot-performance claim.
Materials and Methods > Cell culture, primary AML samples, and treatments (S3); Results > Resistance-associated alterations in protein homeostasis are reverted by PTK2B inhibition (S93, S97); Fig. 2 legend (S190, S192)
Nascent proteomics: Nascent proteomics; comparator: MV4-11R cells with mock treatment (R) — Results > Resistance-associated alterations in protein homeostasis are reverted by PTK2B inhibition (S97); Fig. 2 legend (S190)
