Art. -Nr.: HY-20403

PF-562271 hydrochloride

(Synonyms: VS-6062hydrochloride)

30 Cited Publications

Kundenbewertung

Based on 30 publication(s) in Google Scholar

PF-562271 hydrochloride (VS-6062 hydrochloride) is an orally active, ATP-competitive, reversible FAK/Pyk2 inhibitor, with an IC₅₀ of 1.5 nM for FAK and 13 nM for Pyk2. PF-562271 hydrochloride induces tumor regression, and inhibits tumor growth, invasion and metastasis. PF-562271 hydrochloride exerts no effect on tumor necrosis, angiogenesis or apoptosis in an orthotopic mouse model of pancreatic ductal adenocarcinoma. When combined with Sunitinib (HY-10255A), PF-562271 hydrochloride reduces tumor vascularization, decreases serum alpha-fetoprotein levels and improves cachexia. PF-562271 hydrochloride can be used in research related to prostate cancer, breast cancer, pancreatic cancer, colon cancer, glioblastoma, lung cancer, pancreatic ductal adenocarcinoma and hepatocellular carcinoma.

Nur für Forschungszwecke. Wir verkaufen nicht an Patienten.

Reinheit: 98.10%
CAS. Nr.: 939791-41-0
Formel: C₂₁H₂₁ClF₃N₇O₃S
Molecular Weight:543.95

Speicherung:

4°C, sealed storage, away from moisture

* In solvent : -80°C, 6 months; -20°C, 1 month (sealed storage, away from moisture)

PF-562271 hydrochloride Chemical Structure

CAS. Nr.: 939791-41-0

Größe

Preis

Verfügbarkeit

Menge

Amount: USD 0.00

* Bitte wählen Sie Menge, bevor Sie Artikel hinzufügen.

Top Publications Citing

Use of MCE Products

Fluorescent Dye

Strong Fluorescence Signal / Multi-Disciplinary Applications / High Fluorescence Specificity

Biologische Aktivität
- Beschreibung
- In Vitro
- In Vivo
Chemical Information
Publications (30)
Lösungsmittel & Löslichkeit
- In Vitro
Reinheit & Dokumentation
Verweise
Help & FAQs
Classifications
Bioz

Biologische Aktivität

Beschreibung

In Vitro

PF-562271 hydrochloride potently inhibits purified recombinant FAK (with an IC₅₀ of 1.5 nM) and recombinant Pyk2 (with an IC₅₀ of 13 nM) via ATP-competitive reversible binding^[1].
PF-562271 hydrochloride exhibits over 100-fold selectivity against most tested non-target recombinant kinases, and only shows moderate activity against a subset of cyclin-dependent kinase complexes^[1].
PF-562271 (starting concentration of 1 μM; 30 min) hydrochloride potently and suppresses the autophosphorylation of FAK^Y397 in A431 epithelial cancer cells with an IC₅₀ of 5 nM^[1].
PF-562271 (1.1-3.3 μM; 48 h) hydrochloride alters the cell cycle progression of PC-3M cells only after incubation at the high concentration of 3.3 μM for 48 h^[1].
PF-562271 hydrochloride is an ATP-competitive reversible inhibitor that potently inhibits the kinase activities of purified recombinant FAK (IC₅₀ = 1.5 nM) and PYK2 (IC₅₀ = 14 nM)^[2].
PF-562271 (0.1 μM) hydrochloride significantly inhibits IGF-I-stimulated chemotactic migration of the PDA cell line MPanc-96, but does not affect EGF-stimulated migration of this cell line^[2].

MedChemExpress (MCE) has not independently confirmed the accuracy of these methods. They are for reference only.

ELISA Assay^[1]

Cell Line:

Inducible stable A431 epithelial carcinoma clones expressing wild-type V5-tagged FAK
Concentration:

1 μmol/L (starting concentration, serially diluted)
Incubation Time:

30 min
Result:

Inhibited FAK^Y397 autophosphorylation with an IC₅₀ of 5 nmol/L (2.5 ng/mL).
Showed ~4-fold lower potency for Pyk2 in comparative cell assays.

Cell Cycle Analysis^[1]

Cell Line:

PC-3M human prostate cancer cells
Concentration:

1.1 μmol/L; 3.3 μmol/L
Incubation Time:

48 h
Result:

Reduced the percentage of cells in S and G2-M phases to levels comparable to serum-starved cells at 3.3 μmol/L.
Exerted no effect on cell cycle progression at 1.1 μmol/L.

In Vivo

PF-562271 (3.3-33 mg/kg; p.o.; single dose) hydrochloride inhibits tumor FAK phosphorylation in a dose- and time-dependent manner after oral administration, with an EC₅₀ of 93 ng/mL for whole blood concentrations^[1].
PF-562271 (25-50 mg/kg; p.o.; once daily, twice daily; 15 days) hydrochloride induces dose-dependent tumor growth inhibition in PC-3M xenografts. The efficacy of twice-daily administration is superior to that of once-daily administration at the same total daily dose, and the dose of 50 mg/kg twice daily achieves a TGI of 78% accompanied by partial tumor regression^[1].
PF-562271 (50-100 mg/kg; p.o.; twice daily, once daily; continuous delivery via osmotic minipump) hydrochloride induces significant tumor growth inhibition in BxPc3 xenografts, with the 50 mg/kg twice daily dose achieving 86% TGI and partial tumor regression^[1].
PF-562271 (12.5-50 mg/kg; p.o.; twice daily; for 29 consecutive days) hydrochloride induces dose-dependent tumor growth inhibition in BT474 xenografts, with the 50 mg/kg twice-daily dose achieving a 94% TGI accompanied by partial tumor regression^[1].
PF-562271 (33 mg/kg; twice daily) hydrochloride reduces tumor volume, decreases tumor cell proliferation rate, and significantly lowers the incidence of retroperitoneal invasion and metastasis of orthotopic MPanc-96 pancreatic ductal adenocarcinoma in athymic nude mice^[2].
Combination treatment with PF-562271 (15 mg/kg; p.o.; twice daily; 7 days per week) hydrochloride and Sunitinib (HY-10255A) administered at 20 mg/kg four times daily effectively inhibits hepatocellular carcinoma tumor growth in nude mice, reduces serum AFP and AST levels, impairs tumor angiogenesis, and induces tumor necrosis^[3].

MedChemExpress (MCE) has not independently confirmed the accuracy of these methods. They are for reference only.

Animal Model:

CD-1 Nu/Nu (female, ≈20 grams, U87MG human glioblastoma xenograft model)^[1]
Dosage:

3.3 mg/kg; 10 mg/kg; 33 mg/kg
Administration:

p.o.; single dose
Result:

Achieved 78% maximal inhibition of tumor phospho-FAK at 1 hour postdose, with >50% inhibition sustained for >4 hours (33 mg/kg dose).
Achieved 70% maximal inhibition of tumor phospho-FAK, with >50% inhibition sustained for <2 hours (10 mg/kg dose).
Calculated an EC₅₀ of 93 ng/mL for total blood PF-562271 (mesylate) concentration required for half-maximal reduction of FAK phosphorylation.

Animal Model:

CD-1 Nu/Nu (female, ≈20 grams, PC-3M human prostate xenograft model)^[1]
Dosage:

50 mg/kg (daily); 25 mg/kg (twice daily); 50 mg/kg (twice daily)
Administration:

p.o.; daily; 15 days; p.o.; twice daily; 15 days
Result:

Resulted in 45% tumor growth inhibition (TGI) and 37% inhibition of tumor phospho-FAK after 15 days, with a free Cₘₐₓ of 157 ng/mL (50 mg/kg daily dose).
Resulted in 61% TGI and 27% inhibition of tumor phospho-FAK after 15 days, with a free Cₘₐₓ of 25 ng/mL (25 mg/kg twice daily dose).
Resulted in 78% TGI, 52% inhibition of tumor phospho-FAK after 15 days, regressions in 3/7 mice, a free Cₘₐₓ of 96 ng/mL, and a free Cₐᵥₑ of 16 ng/mL (50 mg/kg twice daily dose).
Caused no weight loss, morbidity, or mortality.

Animal Model:

CD-1 Nu/Nu (female, ≈20 grams, BxPc3 human pancreatic xenograft model)^[1]
Dosage:

50 mg/kg (twice daily); 100 mg/kg (daily); steady-state free concentration of 0.7 ng/mL (continuous delivery)
Administration:

p.o.; twice daily; p.o.; daily; continuous delivery via osmotic mini-pump
Result:

Resulted in 86% TGI, 31% inhibition of tumor phospho-FAK, regressions in 3/10 mice, and a free Cₘₐₓ of 273 ng/mL (50 mg/kg twice daily dose).
Resulted in 71% TGI and 59% inhibition of tumor phospho-FAK, with a free Cₘₐₓ of 705 ng/mL (100 mg/kg daily dose).
Resulted in 57% TGI and 37% inhibition of tumor phospho-FAK (continuous delivery via osmotic mini-pumps).
Caused no weight loss, morbidity, or mortality.

Animal Model:

CD-1 Nu/Nu (female, ≈20 grams, BT474 human breast xenograft model)^[1]
Dosage:

12.5 mg/kg (twice daily); 25 mg/kg (twice daily); 50 mg/kg (twice daily)
Administration:

p.o.; twice daily; 29 days
Result:

Resulted in 37% TGI, 50% inhibition of tumor phospho-FAK, a free Cₘₐₓ of 29 ng/mL, and a free Cₐᵥₑ of 3 ng/mL (12.5 mg/kg twice daily dose).
Resulted in 59% TGI, 55% inhibition of tumor phospho-FAK, regressions in 3/8 mice, a free Cₘₐₓ of 116 ng/mL, and a free Cₐᵥₑ of 14 ng/mL (25 mg/kg twice daily dose).
Resulted in 94% TGI, 76% inhibition of tumor phospho-FAK, regressions in 4/8 mice, a free Cₘₐₓ of 180 ng/mL, and a free Cₐᵥₑ of 40 ng/mL (50 mg/kg twice daily dose).
Caused no weight loss, morbidity, or mortality.

Chemical Information

CAS. Nr. 939791-41-0
Appearance Solid
Molecular Weight 543.95
Formel C₂₁H₂₁ClF₃N₇O₃S
Color Light yellow to yellow
SMILES

CS(=O)(N(C1=NC=CC=C1CNC2=NC(NC3=CC4=C(NC(C4)=O)C=C3)=NC=C2C(F)(F)F)C)=O.[H]Cl
Synonyms

VS-6062hydrochloride
Versand

Room temperature in continental US; may vary elsewhere.
Speicherung

4°C, sealed storage, away from moisture

* In solvent : -80°C, 6 months; -20°C, 1 month (sealed storage, away from moisture)

Publications (30)

All WB

Sort by:

Journal Impact Factor

Nat Biomed Eng

Nonexpansive biodegradable matrix promotes blood vessel organoid development for neurovascular repair and functional recovery in ischaemic stroke. [Abstract]

2025 Nov 3. PMID: 41184604
Cancer Res

High-throughput tyrosine kinase activity profiling identifies FAK as a candidate therapeutic target in Ewing sarcoma. [Abstract]

2013 May 1;73(9):2873-83. PMID: 23536552

PF-562271 hydrochloride purchased from MedChemExpress. Usage Cited in: Cancer Res. 2013 May 1;73(9):2873-83. [Abstract]

FAK inhibition downregulates the AKT/mTOR pathway and CAS activity. A, protein levels measured by Western immunoblotting for AKT/mTOR pathway proteins in A673 and TC32 cells serum-starved overnight, treated with PF-562271 for 6 hours, and then stimulated with IGF-1 for 2 hours. Vinculin is used as the loading control. B, Western immunoblots showing downregulation of phospho-CAS but not phospho-ERK in A673 and TC32 cells after treatment with PF-562271.
Autophagy

PTK2/FAK inhibition triggers TMED9-mediated protective autophagy in pancreatic cancer cell via enhancing ERGIC-ERES contact. [Abstract]

2026 May 29:1-15. PMID: 42144738
Cell Discov

A positive mechanobiological feedback loop controls bistable switching of cardiac fibroblast phenotype. [Abstract]

2022 Sep 6;8(1):84. PMID: 36068215
Carbohydr Polym

Inulin-like polysaccharide ABWW may impede CCl4 induced hepatic stellate cell activation through mediating the FAK/PI3K/AKT signaling pathway in vitro & in vivo. [Abstract]

2024 Feb 15:326:121637. PMID: 38142102
Cell Death Dis

Identification of matrix-remodeling associated 5 as a possible molecular oncotarget of pancreatic cancer. [Abstract]

2023 Feb 24;14(2):157. PMID: 36828810

PF-562271 hydrochloride purchased from MedChemExpress. Usage Cited in: Cell Death Dis. 2023 Feb 24;14(2):157. [Abstract]

PF-562271 (250 nM; 6 h) largely inhibits Akt-S6 phosphorylation in OE-MXRA5 priPC-1 cells.
Cell Death Dis

P130cas-FAK interaction is essential for YAP-mediated radioresistance of non-small cell lung cancer. [Abstract]

2022 Sep 10;13(9):783. PMID: 36088346
Clin Cancer Res

High-throughput Chemical Screening Identifies Focal Adhesion Kinase and Aurora Kinase B Inhibition as a Synergistic Treatment Combination in Ewing Sarcoma. [Abstract]

2019 Jul 15;25(14):4552-4566. PMID: 30979745
Int J Surg

Supervising the recurrence of pancreatic ductal adenocarcinoma using CtDNA-based MIR129-2 methylation detection. [Abstract]

2025 Sep 17. PMID: 40961228
Am J Chin Med

Evodiamine Suppresses Lung Cancer Progression Through Modulating FAK/STAT3/AKT Signaling Pathway. [Abstract]

2025;53(4):1225-1240. PMID: 40582716
World J Gastroenterol

FBP1 as a key regulator of focal adhesion kinase-mediated hepatic stellate cell activation: Multi-omics and experimental validation. [Abstract]

2025 Jul 28;31(28):107361. PMID: 40741470
Cell Rep

Mechanotransduction in response to ECM stiffening impairs cGAS immune signaling in tumor cells. [Abstract]

2023 Oct 5;42(10):113213. PMID: 37804510
Life Sci

Harmine inhibits the proliferation and migration of glioblastoma cells via the FAK/AKT pathway. [Abstract]

2021 Apr 1:270:119112. PMID: 33508300
Breast Cancer Res

TMEM120B strengthens breast cancer cell stemness and accelerates chemotherapy resistance via β1-integrin/FAK-TAZ-mTOR signaling axis by binding to MYH9. [Abstract]

2024 Mar 19;26(1):48. PMID: 38504374
Sci Rep

The mechanical microenvironment regulates ovarian cancer cell morphology, migration, and spheroid disaggregation. [Abstract]

2018 May 8;8(1):7228. PMID: 29740072
Int J Cancer

Targeting FAK scaffold functions inhibits human renal cell carcinoma growth. [Abstract]

2015 Oct 1;137(7):1549-59. PMID: 25809490

PF-562271 hydrochloride purchased from MedChemExpress. Usage Cited in: Int J Cancer. 2015 Oct 1;137(7):1549-59. [Abstract]

786-O (a) and Caki-1 (b) are treated for 24 and 48h with increasing concentrations of PF-562,271 and adherent cells were counted. Cell lysates are evaluated through immunoblotting for total FAK following treatment for 24h.
Cell Signal

Tenvermectin B, a novel macrocyclic lactone antibiotic, suppresses glioblastoma progression by targeting RhoJ. [Abstract]

2025 Sep 10:136:112117. PMID: 40939916
Environ Toxicol Pharmacol

ZC3H4 Governs Epithelial Cell Migration through ROCK/p-PYK2/p-MLC2 Pathway in Silica-induced Pulmonary Fibrosis. [Abstract]

2023 Nov:104:104301. PMID: 37866415
Eur J Cell Biol

The mechanical mechanism of angiotensin II induced activation of hepatic stellate cells promoting portal hypertension. [Abstract]

2024 May 28;103(2):151427. PMID: 38820882
Cancer Med

Focal Adhesion Kinase Intersects With the BRD4-MYC Axis and YAP1 to Drive Tumor Cell Growth, Phenotypic Plasticity, Stemness, and Metastatic Potential in Colorectal Cancer. [Abstract]

2025 Sep;14(18):e71227. PMID: 40959971
Mol Biol Rep

Piperlongumine inhibits the proliferation and migration of non-small cell lung cancer cells through the EGFR/FAK/STAT3 pathway. [Abstract]

2026 May 14;53(1):770. PMID: 42133146
Mol Biol Rep

Ginkgetin inhibits the proliferation and migration of lung cancer cells via FAK/STAT3/AKT pathway. [Abstract]

2025 May 14;52(1):458. PMID: 40366441
J Nat Med

Antiangiogenic effects of AG36, a triterpenoid saponin from Ardisia gigantifolia stapf. [Abstract]

2020 Sep;74(4):732-740. PMID: 32643027
Anticancer Drugs

AZD7762 induces CRBN dependent BAG3 degradation through ubiquitin-proteasome pathway. [Abstract]

2024 Jan 1;35(1):46-54. PMID: 37449977
Res Sq

2025 Jul 11.
bioRxiv

2025 May 28.
bioRxiv

FAK Differentially Mechanoregulates Cell Migration During Wound Closure. [Abstract]

2025 Apr 7:2025.04.01.646098. PMID: 40291676
Research Square Preprint

2023 May 23.
Research Square Preprint

2021 Dec.
Practical Oncology Journal

2015, 29(5): 444-449.

PF-562271 hydrochloride purchased from MedChemExpress. Usage Cited in: Practical Oncology Journal. 2015, 29(5): 444-449.

Effects and mechanism of Biglycan and FAK signaling pathway on the invasion and metastasis of colon cancer cells.

Lösungsmittel & Löslichkeit

In Vitro:

DMSO : 100 mg/mL (183.84 mM; Need ultrasonic; Hygroscopic DMSO has a significant impact on the solubility of product, please use newly opened DMSO)

View the Complete Stock Solution Preparation Table

Preparing Stock Solutions

View the Complete Stock Solution Preparation Table

Concentration Solvent Mass

1 mg

5 mg

10 mg

Concentration

Solvent

Mass

1 mM

1.8384 mL

9.1920 mL

18.3840 mL

5 mM

0.3677 mL

1.8384 mL

3.6768 mL

10 mM

0.1838 mL

0.9192 mL

1.8384 mL

Please refer to the solubility information to select the appropriate solvent. Once prepared, please aliquot and store the solution to prevent product inactivation from repeated freeze-thaw cycles.

Storage method and period of stock solution: -80°C, 6 months; -20°C, 1 month (sealed storage, away from moisture). When stored at -80°C, please use it within 6 months. When stored at -20°C, please use it within 1 month.

Molaritätsrechner

Mass (g) = Concentration (mol/L) × Volume (L) × Molecular Weight (g/mol)

Mass Mass

Konzentration Konzentration

Volumen Volumen

Molecular Weight Molecular Weight

Verdünnungsrechner

Konzentration _{(Stammlösung)} × Volumen _{(Stammlösung)} = Konzentration _{(Ziellösung)} × Volumen _{(Ziellösung)}

Konzentration _{(Stammlösung)} Konzentration _{(Stammlösung)}

Volumen _{(Stammlösung)} Volumen _{(Stammlösung)}

Konzentration _{(Ziellösung)} Konzentration _{(Ziellösung)}

Volumen _{(Ziellösung)} Volumen _{(Ziellösung)}

Reinheit & Dokumentation

Select Batch:

Reinheit: 99.98%

Assay: 99.98%

ee.: 99.98%

Data Sheet (286 KB)
SDS (252 KB)
- English - EN (252 KB)
- Français - FR (252 KB)
- Deutsch - DE (252 KB)
- Norwegian - NO (252 KB)
- Español - ES (252 KB)
- Swedish - SV (252 KB)
- Italian - IT (252 KB)
- Korean - KR (252 KB)
- Portuguese - PT (252 KB)
COA (2659 KB)
Elemental Analysis Report (2659 KB)
HNMR (2659 KB)
CNMR (2659 KB)
RP-HPLC (2659 KB)
NP-HPLC (2659 KB)
MS (2659 KB)
LCMS (2659 KB)
IR (2659 KB)
GC (2659 KB)
OR (2659 KB)
SDS-PAGE (2659 KB)
SEC-HPLC (2659 KB)
Other Report (2659 KB)
Handling Instructions (2659 KB)

Verweise

[1]. Roberts WG, et al. Antitumor activity and pharmacology of a selective focal adhesion kinase inhibitor, PF-562,271. Cancer research. 2008 Mar 15;68(6):1935-44. [Content Brief]

[2]. Stokes JB, 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 Nov;10(11):2135-45. [Content Brief]

[3]. Bagi CM, et al. Sunitinib and PF-562,271 (FAK/Pyk2 inhibitor) effectively block growth and recovery of human hepatocellular carcinoma in a rat xenograft model. Cancer biology & therapy. 2009 May;8(9):856-65. [Content Brief]

Help & FAQs

How should lyophilized recombinant proteins be reconstituted and stored?

1. Before opening the cap, centrifuge the vial at 13000 rpm for 20-30 seconds. This step will ensure that any lyophilized powder that may have adhered to the cap or walls is collected at the bottom of the vial, minimizing the risk of product loss.

Complete Stock Solution Preparation Table

Optional Solvent	Concentration Solvent Mass	1 mg	5 mg	10 mg	25 mg
DMSO	1 mM	1.8384 mL	9.1920 mL	18.3840 mL	45.9601 mL
	5 mM	0.3677 mL	1.8384 mL	3.6768 mL	9.1920 mL
	10 mM	0.1838 mL	0.9192 mL	1.8384 mL	4.5960 mL
	15 mM	0.1226 mL	0.6128 mL	1.2256 mL	3.0640 mL
	20 mM	0.0919 mL	0.4596 mL	0.9192 mL	2.2980 mL
	25 mM	0.0735 mL	0.3677 mL	0.7354 mL	1.8384 mL
	30 mM	0.0613 mL	0.3064 mL	0.6128 mL	1.5320 mL
	40 mM	0.0460 mL	0.2298 mL	0.4596 mL	1.1490 mL
	50 mM	0.0368 mL	0.1838 mL	0.3677 mL	0.9192 mL
	60 mM	0.0306 mL	0.1532 mL	0.3064 mL	0.7660 mL
	80 mM	0.0230 mL	0.1149 mL	0.2298 mL	0.5745 mL
	100 mM	0.0184 mL	0.0919 mL	0.1838 mL	0.4596 mL

Keywords

PF-562271 hydrochloride

30 Cited Publications

100 mg Angebot einholen

Subscribe to the

MedChemExpress

Newsletter

Produktname:
Art. -Nr.:
Menge:
MCE Japan Authorized Agent:

Produktname:
CAS. Nr.:
Species:
Reinheit:
Menge:

PF-562271 hydrochloride

Bioactive Compound Library Max

Bioactive Compound Library

Kinase Inhibitor Library

Protein Tyrosine Kinase Compound Library

Anti-Cancer Compound Library

Cytoskeleton Compound Library

Anti-Pancreatic Cancer Compound Library

Anti-Pulmonary Fibrosis Compound Library

Heterocyclic Compound Library

Multi-Target Compound Library

MCE Bioactive Compound Library

Protein Kinase Compound Library

High-Throughput Bioactive Compound Library

Publications Citing Use of MedChemExpress (MCE) PF-562271 hydrochloride

Biologische Aktivität

Chemical Information

Publications (30)

Lösungsmittel & Löslichkeit

Reinheit & Dokumentation

Verweise

Help & FAQs

Complete Stock Solution Preparation Table

PF-562271 hydrochloride

Bioactive Compound Library Max

Bioactive Compound Library

Kinase Inhibitor Library

Protein Tyrosine Kinase Compound Library

Anti-Cancer Compound Library

Cytoskeleton Compound Library

Anti-Pancreatic Cancer Compound Library

Anti-Pulmonary Fibrosis Compound Library

Heterocyclic Compound Library

Multi-Target Compound Library

MCE Bioactive Compound Library

Protein Kinase Compound Library

High-Throughput Bioactive Compound Library

Publications Citing Use of MedChemExpress (MCE) PF-562271 hydrochloride

Biologische Aktivität

Chemical Information

Publications (30)

Lösungsmittel & Löslichkeit

Reinheit & Dokumentation

Verweise

Help & FAQs

Complete Stock Solution Preparation Table

PF-562271 hydrochloride Related Classifications

HY-20403 Related Classifications