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Fig. 1 · Structure
Cat. No.
A11192
CAS No.
717907-75-0
Formula
C21H20F3N7O3S
Mol. Weight
507.49

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PF-562271

Cat. No. A11192 CAS 717907-75-0

FAK inhibitor

PF-562271 is an orally bioavailable small molecule and ATP-competitive focal adhesion kinase (FAK) inhibitor with potential antineoplastic and antiangiogenic activities.

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Publications for PF-562271

1 publication citing this product

  1. Jiping Yue, .et al. , Nat Commun, 2016, 7: 11692 PMID: 27216888
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Biological Activity

Bioactivity / Mechanism

PF-562271 suppresses cellular FAK phosphorylation. In expanded primary human T cells, 10 μM PF-562,271 reduced TCR-induced phosphorylation at FAK Y397, Y576/577 and Y925 relative to stimulated DMSO controls. This fixed-concentration cellular result does not establish an enzyme IC50 or exclusive FAK-mediated activity. [1]

Literature-reported observations and conditions; not Adooq-tested protocols or general treatment recommendations.

Target & Activity

Target Activity Value
FAK IC50 1.5nM
PYK2 IC50 13nM
CDK2/CyclinE IC50 30nM
CDK3/CyclinE IC50 47nM
CDK1/CyclinB IC50 58nM
CDK7/CyclinH/MAT1 IC50 97nM
FLT3 IC50 97nM
GSK-3α IC50 101nM
CDK5/p35 IC50 120nM
GSK-3β IC50 133nM
AuroraA IC50 145nM
CDK2/CyclinA IC50 227nM
YES IC50 294nM
MAPK1 IC50 340nM
Fyn IC50 377nM
LCK IC50 408nM
IGF-1R IC50 >500nM
PKA IC50 620nM
c-Src IC50 797nM
CDK4 IC50 >1μM
CDK6/CyclinD2 IC50 >1μM
Chk1 IC50 >1μM
Chk2 IC50 >1μM
EGFR IC50 >1μM
EphB2 IC50 >1μM
FGFR3 IC50 >1μM
Abl IC50 >1μM
Fms IC50 >1μM
IKKα IC50 >1μM
IKKβ IC50 >1μM
JNK1α1 IC50 >1μM
MEK1 IC50 >1μM
p70S6K IC50 >1μM
PKBα IC50 >1μM
PKBβ IC50 >1μM
PKBγ IC50 >1μM
PKCα IC50 >1μM
PKCβ2 IC50 >1μM
PKCδ IC50 >1μM
TrkB IC50 >2.5μM
PDGFRβ IC50 >3μM

41 targets · Scroll to view more

Cellular Effect

Cell Line Activity Value Description Reference
A375P GI50 10.22 μM Antiproliferative activity against human A375P cells assessed as growth inhibition measured after 72 hrs by CellTiter-Glo assay [PMID: 34324343]
HCT-116 GI50 1.14 μM Antiproliferative activity against human HCT-116 cells assessed as growth inhibition measured after 72 hrs by CellTiter-Glo assay [PMID: 34324343]
MDA-MB-231 GI50 1.95 μM Antiproliferative activity against human MDA-MB-231 cells assessed as growth inhibition measured after 72 hrs by CellTiter-Glo assay [PMID: 34324343]
Sf9 IC50 1.5 nM Reversible/competitive inhibition of NH2-terminal His6-tagged FAK kinase domain (410 to 689 residues) (unknown origin) expressed in baculovirus infected sf9 cells using p(Glu/Tyr) as substrate in presence of ATP [PMID: 27876318]
SMMC-7721 IC50 23.92 μM Antiproliferative activity against human SMMC-7721 cells assessed as inhibition of cell growth measured after 48 hrs by MTT assay [PMID: 34214842]

In Vitro Studies

In pancreatic cancer cultures, responses depended on the endpoint. At 0.1 μM, PF-562,271 reduced IGF-I-driven migration, collagen-I-directed migration and serum-stimulated invasion of MPanc-96 cells, whereas EGF-driven migration was insensitive. The paper also reported no inhibition of PDA-cell proliferation up to 1 μM and no enhancement of gemcitabine-mediated growth inhibition under its culture conditions. [2]

PF-562,271 inhibited stimulated proliferation of cultured mouse CD4+ T cells over 72 hours. PMA/ionomycin bypass of proximal TCR signaling restored proliferation in PP2-treated cells but did not restore it in PF-562,271-treated cells, indicating that the antiproliferative response extends beyond proximal TCR signaling. [1]

Cellular FAK phosphorylation in human T cells

Cell-based study · Primary human peripheral-blood CD4+ T cells, expanded before testing [1]

PF-562,271 reduced TCR-induced phosphorylation of FAK at Y397, Y576/577 and Y925. PP2 produced a stronger suppression; basal Y925 phosphorylation also decreased significantly with PF-562,271.

Measured endpoints — not treatment concentrations
EndpointReported resultReference
TCR-induced FAK Y397, Y576/577 and Y925 phosphorylationphosphorylation relative to total FAK Reduced relative to TCR-stimulated DMSO controls; mean ± SD, n=3 independent experiments; ANOVA significance markers p < 0.05 in Figure 1D/F.[1]

Literature-Reported Treatment Conditions

Treatment concentration
10 μM
Exposure duration
30 min compound pretreatment; 7 min stimulation on OKT3-coated plates for the FAK assay
Method
Immunoblotting of phospho-FAK relative to total FAK
Vehicle
DMSO; final percentage not specified in the adopted locations
Co-treatment
No therapeutic combination; TCR stimulation and PP2 comparator controls
Reported limits
No kinase IC50 is estimated from this fixed-concentration cellular assay.
Methods and source locations

Compound reported in the paper: PF-562,271

Evidence applies to the named compound and tested material; no salt conversion, cross-supplier equivalence or Adooq lot validation is established.

Figure 1C–F and caption; Methods 2.1, 2.2, 2.8; Results 3.1

TCR-induced FAK Y397, Y576/577 and Y925 phosphorylation: Site-specific immunoblotting; unstimulated and stimulated DMSO controls, PP2 comparator — Figure 1C–F and caption; Methods 2.1, 2.2, 2.8; Results 3.1

Stimulated proliferation of mouse CD4+ T cells

Cell-based study · OVA-expanded OTII+ mouse CD4+ T cells in culture [1]

PF-562,271 inhibited stimulated proliferation. Bypassing proximal TCR signaling with PMA/ionomycin restored proliferation with PP2 but did not restore it with PF-562,271.

Measured endpoints — not treatment concentrations
EndpointReported resultReference
Stimulated CD4+ T-cell proliferative indexproliferative index Dose-dependent inhibition with bead or antigen stimulation; inhibition persisted with PMA/ionomycin at 5 μM. Mean ± SD from 3 independent experiments; Figure 7A–C marks p < 0.05.[1]

Literature-Reported Treatment Conditions

Treatment concentration
0.2, 1 and 5 μM
Exposure duration
72 h
Method
CFSE dye dilution by flow cytometry; proliferative index by ModFIT
Vehicle
DMSO
Co-treatment
No therapeutic combination. Separate stimuli: anti-CD3/CD28 beads, antigen-loaded splenocytes, or PMA/ionomycin. PP2 comparator.
Reported limits
This is a cultured-cell experiment, not an animal drug-treatment study.
Methods and source locations

Compound reported in the paper: PF-562,271

Evidence applies to the named compound and tested material; no salt conversion, cross-supplier equivalence or Adooq lot validation is established.

Figure 7A–C and caption; Methods 2.1, 2.2, 2.7; Results 3.8–3.9; Discussion

Stimulated CD4+ T-cell proliferative index: CFSE dilution among viable gated CD4+ cells; unstimulated, stimulated DMSO and PP2 controls — Figure 7A–C and caption; Methods 2.1, 2.2, 2.7; Results 3.8–3.9; Discussion

Stimulus-dependent pancreatic cancer migration and invasion

Cell-based study · MPanc-96 human pancreatic ductal adenocarcinoma cells [2]

At 0.1 μM, PF-562,271 reduced IGF-I-driven and collagen-I-directed migration and serum-stimulated invasion. EGF-driven migration was insensitive under these conditions.

Measured endpoints — not treatment concentrations
EndpointReported resultReference
Stimulus-dependent migration and serum-stimulated invasioncells/field (qualitative group comparison) IGF-I migration, collagen-I haptotaxis and serum invasion decreased (p < 0.05 in Figure 3A); EGF migration was insensitive. Bars represent standard error; n not stated in caption.[2]

Literature-Reported Treatment Conditions

Treatment concentration
0.1 μM
Exposure duration
Treatment/assay duration not specified in the retrieved main-text methods or Figure 3A caption
Method
Transwell migration; Matrigel inserts for invasion
Vehicle
Matched absence-of-inhibitor controls; vehicle identity not specified for these assays in adopted locations
Co-treatment
No therapeutic combination. IGF-I (100 ng/mL), EGF (25 ng/mL), collagen-I or serum were separate assay stimuli.
Reported limits
Pretreatment is described for haptotaxis/invasion, without a duration. Do not borrow timing from referenced protocols.
Methods and source locations

Compound reported in the paper: PF-562,271

Evidence applies to the named compound and tested material; no salt conversion, cross-supplier equivalence or Adooq lot validation is established.

Figure 3A and caption; Results: PDA cell receptor signaling, migration and invasion; Methods: transwell migration, invasion and proliferation assays; PF-562,271 and gemcitabine treatment

Stimulus-dependent migration and serum-stimulated invasion: Transwell assays with unstimulated/uncoated controls and matched stimulated inhibitor-free conditions — Figure 3A and caption; Results: PDA cell receptor signaling, migration and invasion; Methods: transwell migration, invasion and proliferation assays; PF-562,271 and gemcitabine treatment

Limited antiproliferative response in pancreatic cancer cultures

Cell-based study · Human pancreatic ductal adenocarcinoma cell cultures; Results discusses MPanc-96 and MAD08-608 together [2]

The main text reports no proliferation inhibition by PF-562,271 up to 1 μM and no enhancement of gemcitabine-mediated growth inhibition. Model-specific supplementary data were not separately adopted.

Measured endpoints — not treatment concentrations
EndpointReported resultReference
Cell number with PF-562,271 alone or with gemcitabinecell number (negative PF-562,271 response) No effect on proliferation up to 1 μM in Results; no enhancement of gemcitabine effect. Gemcitabine itself inhibited cell growth; Figure 3C bars denote standard error, n not stated.[2]

Literature-Reported Treatment Conditions

Treatment concentration
PF-562,271 up to 1 μM for the text-supported negative conclusion
Exposure duration
Assay duration not specified in retrieved main methods or Figure 3C caption
Method
CyQuant cell-number assay in 1% FBS-containing medium
Vehicle
Inhibitor-free culture control; vehicle identity not specified in the adopted locations
Co-treatment
Separate PF-562,271-alone and PF-562,271 plus gemcitabine conditions; gemcitabine 1, 10 or 100 ng/mL
Reported limits
Main Figure 3C is not independently labeled by cell line; main text identifies both lines and refers to supplementary data. The adopted conclusion is restricted to the stated PDA culture conditions, without per-line numerical estimates.
Methods and source locations

Compound reported in the paper: PF-562,271

Evidence applies to the named compound and tested material; no salt conversion, cross-supplier equivalence or Adooq lot validation is established.

Figure 3C and caption; Results: final paragraph of PDA cell receptor signaling, migration and invasion; Methods: transwell migration, invasion and proliferation assays; PF-562,271 and gemcitabine treatment

Cell number with PF-562,271 alone or with gemcitabine: CyQuant assay; inhibitor-free and gemcitabine-alone comparators — Figure 3C and caption; Results: final paragraph of PDA cell receptor signaling, migration and invasion; Methods: transwell migration, invasion and proliferation assays; PF-562,271 and gemcitabine treatment

In Vivo Studies

In PC3M-luc-C6 subcutaneous xenografts, oral PF-562,271 at 25 mg/kg twice daily, 5 days per week for 2 weeks, produced a reported 62% tumor growth inhibition at day 14. The caliper-based group difference did not persist after treatment. Bioluminescence differed significantly only on day 11; two treated mice were later euthanized for tumor ulceration. [3]

In a separate PC3M-luc-C6 metastatic xenograft experiment using the same dose with a planned 3-week course, the day-18 mean dorsal lesion signal increased less with PF-562,271 than vehicle (2,854% versus 14,190%; p = 0.006). The largest-lesion analysis was not significant (p = 0.07), with only three analyzed mice per group after baseline exclusions. These analysis-dependent imaging results support a limited preclinical conclusion. [3]

Local-implant prostate xenograft growth and imaging

Animal study · Male BALB/cAnNCr-nu/nu mice with PC3M-luc-C6 subcutaneous tumors [3]

PF-562,271 slowed tumor growth during treatment. The BLI difference was significant only on day 11; caliper group differences did not persist after treatment.

Measured endpoints — not treatment concentrations
EndpointReported resultReference
Caliper tumor growth at day 14percent growth inhibition and percent change from baseline 62% tumor growth inhibition reported. Tumor-size increase: treated 40% (±47), control 110% (±19); p < 0.05. Figure 1 error bars denote SD.[3]
BLI signal increase at day 11percent change from baseline Treated 88% (±49) versus control 490% (±199), p < 0.05; significant only on day 11. Day-14 difference not significant. Figure 2 error bars denote SD.[3]

Conditions shared by the study groups

Route
Oral (p.o.)
Frequency
Twice daily on 5 days/week (reported as BID, 5x/wk)
Treatment course
2 weeks
Vehicle
Drug stock in 50% DMSO/50% PEG-400, then diluted in sterile saline before dosing; final DMSO/PEG percentages not stated
Study groups and reported outcomes
Group / doseComparatorObserved resultReference
PF-562,271 local-implant group
25 mg/kg		Vehicle group n=4; treated n=5 randomized mice; one mouse per group excluded for BLI due to large initial tumor sizeReported 62% tumor growth inhibition at day 14. Significance in caliper tumor growth did not persist after treatment. Two treated mice were euthanized on days 16 and 18 for tumor ulceration.[3]
PF-562,271 local-implant group
Model: Male BALB/cAnNCr-nu/nu mice bearing PC3M-luc-C6 subcutaneous xenografts
Reported limits: BLI analysis therefore used fewer mice than randomized; final vehicle composition is not explicitly quantified.
Methods and source locations

Compound reported in the paper: PF-562,271

Evidence applies to the named compound and tested material; no salt conversion, cross-supplier equivalence or Adooq lot validation is established.

Results: Efficacy study and Bioluminescent imaging study in subcutaneously inoculated xenograft model; Figures 1–2 and captions; Methods and Materials: Drugs, Animals, Local implant model, Statistical analysis, Bioluminescent imaging study

Caliper tumor growth at day 14: Caliper volumes normalized to each animal’s day-0 tumor volume — Results: Efficacy study and Bioluminescent imaging study in subcutaneously inoculated xenograft model; Figures 1–2 and captions; Methods and Materials: Drugs, Animals, Local implant model, Statistical analysis, Bioluminescent imaging study

BLI signal increase at day 11: BLI with pretreatment baseline; one mouse per group excluded; day-14 control signal loss possibly due to necrosis according to authors — Results: Efficacy study and Bioluminescent imaging study in subcutaneously inoculated xenograft model; Figures 1–2 and captions; Methods and Materials: Drugs, Animals, Local implant model, Statistical analysis, Bioluminescent imaging study

PF-562,271 local-implant group · Results: Efficacy study and Bioluminescent imaging study in subcutaneously inoculated xenograft model; Figures 1–2 and captions; Methods and Materials: Drugs, Animals, Local implant model, Statistical analysis, Bioluminescent imaging study

Analysis-dependent response in a prostate metastasis imaging model

Animal study · Male BALB/cAnNCr-nu/nu mice with PC3M-luc-C6 disseminated xenograft lesions [3]

Treatment reduced the day-18 increase in mean dorsal lesion signal, but the largest-lesion-per-mouse analysis did not reach significance. Small samples and imaging limitations restrict interpretation.

Measured endpoints — not treatment concentrations
EndpointReported resultReference
Day-18 dorsal BLI, average signal across lesions per mousepercent change from baseline Treated 2,854% versus vehicle 14,190% change from baseline; p = 0.006; n=3 mice/group after exclusions. Figure 5 error bars denote SD.[3]
Day-18 dorsal BLI, largest lesion per mousepercent change from baseline Treated 2,938% versus vehicle 13,520%; p = 0.07 (not significant); n=3 mice/group. Ventral imaging difference also not significant (data not shown).[3]

Conditions shared by the study groups

Route
Oral (p.o.)
Frequency
Twice daily on 5 days/week (reported as BID, 5x/wk)
Treatment course
3-week planned course; analyzed results through day 18
Vehicle
Drug stock in 50% DMSO/50% PEG-400, then diluted in sterile saline before dosing; final DMSO/PEG percentages not stated
Study groups and reported outcomes
Group / doseComparatorObserved resultReference
PF-562,271 metastatic-model group
25 mg/kg		Vehicle and PF-562,271 groups initially n=5 each; two mice per group excluded for no dorsal baseline signal; analyzed n=3/groupAt day 18, mean-lesion dorsal BLI favored treatment (p=0.006), but largest-lesion analysis was not significant (p=0.07). Ventral imaging differences were not significant.[3]
PF-562,271 metastatic-model group
Model: Male BALB/cAnNCr-nu/nu mice with PC3M-luc-C6 disseminated lesions
Reported limits: Day-24 data insufficient after a vehicle-group death. Figure 5 uses day-1 baseline, whereas general methods describe day-0 pretreatment imaging; retain this endpoint-specific distinction.
Methods and source locations

Compound reported in the paper: PF-562,271

Evidence applies to the named compound and tested material; no salt conversion, cross-supplier equivalence or Adooq lot validation is established.

Results: BLI study in intra-cardiac inoculated metastasis xenograft model; Figure 5A–B and caption; Methods and Materials: Drugs, Animals, Metastasis model, Statistical analysis, Bioluminescent imaging study

Day-18 dorsal BLI, average signal across lesions per mouse: Mean-lesion-per-mouse analysis; Figure 5A specifies day-1 baseline — Results: BLI study in intra-cardiac inoculated metastasis xenograft model; Figure 5A–B and caption; Methods and Materials: Drugs, Animals, Metastasis model, Statistical analysis, Bioluminescent imaging study

Day-18 dorsal BLI, largest lesion per mouse: Largest-lesion analysis, Figure 5B; ventral data described only in Results — Results: BLI study in intra-cardiac inoculated metastasis xenograft model; Figure 5A–B and caption; Methods and Materials: Drugs, Animals, Metastasis model, Statistical analysis, Bioluminescent imaging study

PF-562,271 metastatic-model group · Results: BLI study in intra-cardiac inoculated metastasis xenograft model; Figure 5A–B and caption; Methods and Materials: Drugs, Animals, Metastasis model, Statistical analysis, Bioluminescent imaging study

Specifications

Manufacturer Adooq Bioscience
Actions Inhibitor
CAS Number 717907-75-0
Applications FAK inhibitor
Formula C21H20F3N7O3S
Molecular Weight 507.49
SMILES
CN(C1=C(C=CC=N1)CNC2=NC(=NC=C2C(F)(F)F)NC3=CC4=C(C=C3)NC(=O)C4)S(=O)(=O)C

Storage & Solubility

In Vitro Solubility

Reported Solubility

SolventReported Solubility
DMSO Warmed: 91 mg/mL (179.31 mM)
Water Insoluble
Ethanol Insoluble

Preparing Stock Solutions

Stock preparation is unavailable for this product molecular weight.

Calculated stock concentrations do not establish solvent solubility. Refer to the reported solubility data for experimental guidance.

In Vivo Preparation

Concentration
4 mg/mL
Vehicle
5% DMSO+40% PEG 300+5% Tween 80+50% ddH2O

Storage

Store powder at -20°C, keep desiccated.
In powder form, the chemical is stable for 36 months.
In solution, store at -20°C and use within 1 month to prevent loss of potency. Aliquot to avoid multiple freeze/thaw cycles.

Research References

  1. [1] Andrew J Wiemer, Sarah A Wernimont, Thai-duong Cung, et al. The focal adhesion kinase inhibitor PF-562,271 impairs primary CD4+ T cell activation Biochemical pharmacology (2013). PMID: 23928188 DOI: 10.1016/j.bcp.2013.07.024 Source material
  2. [2] Jayme B Stokes, Sara J Adair, Jill K Slack-Davis, et al. Inhibition of Focal Adhesion Kinase by PF-562,271 Inhibits the Growth and Metastasis of Pancreatic Cancer Concomitant with Altering the Tumor Microenvironment Molecular cancer therapeutics (2011). PMID: 21903606 DOI: 10.1158/1535-7163.MCT-11-0261 Source material
  3. [3] Haihao Sun, Stephen Pisle, Erin R Gardner, et al. Bioluminescent imaging study: FAK inhibitor, PF-562,271, preclinical study in PC3M-luc-C6 local implant and metastasis xenograft models Cancer Biology & Therapy (2010). PMID: 20495381 DOI: 10.4161/cbt.10.1.11993 Source material

Publications

1 publication citing this product

  1. Jiping Yue, .et al. , Nat Commun, 2016, 7: 11692 PMID: 27216888

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