| Field | Specification |
|---|---|
| Alternative names | VS-6063 hydrochloride; PF 04554878 hydrochloride |
| CAS no. | |
| Applications | |
| Molecular weight | |
| Molecular formula | C20H22ClF3N8O3S |
| Purity | |
| SMILES | |
| Form | Solid |
| Storage | |
| Shipping | |
| Catalog no. (Mfr.) | |
| Main SKU |
Compound Overview
Defactinib hydrochloride, also known as VS-6063 hydrochloride or PF 04554878 hydrochloride, is a FAK inhibitor that inhibits FAK phosphorylation at the Tyr397 site in a time- and dose-dependent manner. It is supplied as a white to off-white solid (C20H22ClF3N8O3S, MW 546.95) at 99.35% purity.
Physical & Chemical Properties
| CAS Number | 1073160-26-5 |
|---|---|
| Molecular Formula | C20H22ClF3N8O3S |
| Molecular Weight | 546.95 g/mol |
| Purity | 99.35% |
| Appearance | Solid |
| Color | White to off-white |
| SMILES | O=C(NC)C1=CC=C(NC2=NC=C(C(F)(F)F)C(NCC3=NC=CN=C3N(C)S(=O)(C)=O)=N2)C=C1.[H]Cl |
| Signaling Pathway | Protein Tyrosine Kinase/RTK |
| Solubility | In Vitro: DMSO: 6.67 mg/mL (12.19 mM; Requires sonication; Hygroscopic DMSO has a significant impact on the solubility of product, please use newly opened DMSO) H2O: < 0.1 mg/mL (insoluble) |
| Storage | 4°C, sealed storage, away from moisture. In solvent: -80°C, 6 months; -20°C, 1 month (sealed storage, away from moisture). |
| Shipping | Room temperature in continental US; may vary elsewhere. |
Literature Cited
Sources cited in this description and in the In Vitro & In Vivo Data tab. Peer-reviewed publications that used this product are listed under References.
Safety
For Research Use Only. Not for use in diagnostic or therapeutic procedures, and not for human or veterinary use. Handle in accordance with the Safety Data Sheet and your institution's chemical hygiene plan.
In Vitro
| Solvent | Solubility | Notes |
|---|---|---|
| DMSO | 6.67 mg/mL (12.19 mM) | requires sonication; use freshly opened DMSO (absorbed moisture lowers solubility) |
| H2O | < 0.1 mg/mL | insoluble |
Aliquot the stock solution and store it at -80°C (up to 6 months) or -20°C (up to 1 month); sealed storage, away from moisture; avoid repeated freeze-thaw cycles.
In Vivo
Choose the formulation that suits the animal model and route of administration; percentages are volume ratios of the final working solution. Start from a clear DMSO stock (see In Vitro above), add the co-solvents one at a time in the order listed, mixing after each addition, and prepare the working solution fresh on the day of dosing. If precipitation or phase separation occurs, gentle warming or sonication can help.
Protocol 1
| Composition | 10% DMSO + 40% PEG300 + 5% Tween-80 + 45% saline |
|---|---|
| Result | ≥ 0.67 mg/mL (1.22 mM); clear solution |
| How to prepare | Gives a clear solution at ≥ 0.67 mg/mL (saturation not determined). For 1 mL of working solution: add 100 μL DMSO stock (6.7 mg/mL) to 400 μL PEG300; then 50 μL Tween-80; then 450 μL saline to bring the volume to 1 mL. Saline: dissolve 0.9 g sodium chloride in ddH2O and make up to 100 mL. |
Protocol 2
| Composition | 10% DMSO + 90% (20% SBE-β-CD in saline) |
|---|---|
| Result | ≥ 0.67 mg/mL (1.22 mM); clear solution |
| How to prepare | Gives a clear solution at ≥ 0.67 mg/mL (saturation not determined). For 1 mL of working solution: add 100 μL DMSO stock (6.7 mg/mL) to 900 μL 20% SBE-β-CD in saline. 20% SBE-β-CD in saline: dissolve 2 g SBE-β-CD powder in 10 mL saline until clear (4°C, store up to one week). |
Protocol 3
| Composition | 10% DMSO + 90% Corn Oil |
|---|---|
| Result | ≥ 0.67 mg/mL (1.22 mM); clear solution |
| How to prepare | Gives a clear solution at ≥ 0.67 mg/mL (saturation not determined). Use with caution if continuous dosing will exceed two weeks. For 1 mL of working solution: add 100 μL DMSO stock (6.7 mg/mL) to 900 μL corn oil. |
Protocol 4
| Composition | 2% DMSO + 40% PEG300 + 5% Tween-80 + 53% saline |
|---|---|
| Result | ≥ 0.5 mg/mL (0.91 mM); clear solution |
Data provided by the manufacturer.
In Vitro
Defactinib (VS-6063) inhibits FAK phosphorylation at Tyr397 in a time- and dose-dependent manner. RPPA data show reduced levels of AKT and YB-1 with Defactinib in taxane-resistant cell lines. Defactinib inhibits expression of pFAK (Tyr397) in all cell lines in a statistically significant, dose-dependent manner. Within 3 hours, Defactinib inhibits pFAK (Tyr397) expression, which gradually returns by 48 hours[1].
In Vivo
At 3 hours, pFAK (Tyr397) is statistically significantly inhibited by Defactinib (VS-6063) doses of 25 mg/kg twice a day or greater, and expression is seen to return by 24 hours. Defactinib at 25 mg/kg twice a day is therefore selected as the dosing schedule for subsequent therapy experiments. Therapy experiments use female nude mice with HeyA8 tumors in the peritoneal cavity, split at random into 4 groups (n=10 per group): 1) control, with vehicle orally twice daily and phosphate-buffered saline intraperitoneally weekly; 2) Defactinib at 25 mg/kg, given orally twice daily; 3) PTX, given intraperitoneally weekly; and 4) Defactinib at 25 mg/kg orally twice daily together with PTX given intraperitoneally weekly. In the HeyA8 model, PTX monotherapy gives an 87.4% reduction in tumor weight, and combination therapy gives the greatest tumor weight reduction, 97.9% (P=0.05 compared with PTX). In the SKOV3ip1 model, the combination group shows a 92.7% tumor weight reduction relative to PTX (P<0.001)[1].
Data provided by the manufacturer. Numbered citations refer to the Literature Cited list in the product description.
Animal Administration[1]
Mice[1] To determine the antitumor effects of Defactinib, inject SKOV3ip1, SKOV3-TR, HeyA8, and HeyA8-MDR cells intraperitoneally. One week after tumor cell injection, randomly assign the mice to 4 groups of 10 mice (control; PTX alone; Defactinib alone; PTX combined with Defactinib), and start treatment 3-4 weeks following injection. Give PTX intraperitoneally every week at 2 mg/kg (SKOV3ip1 and SKOV3-TR) or 2.5 mg/kg (HeyA8 and HeyA8-MDR), and give Defactinib orally at 25 mg/kg twice every day. Give control mice HBSS intraperitoneally once a week and vehicle by mouth twice every day. Check the mice daily for adverse effects of therapy and kill them on day 35 (SKOV3ip1 or SKOV3-TR) or day 28 (HeyA8 or HeyA8-MDR), or when any mouse seems moribund. Record total body weight, tumor incidence and mass, and number of tumor nodules. Fix tumors in formalin, embed them in paraffin, or snap freeze them in optimal cutting temperature (OCT) compound in liquid nitrogen.
Data provided by the manufacturer. Numbered citations refer to the Literature Cited list in the product description.
Need this compound in a format that drops straight into your assay? We can tailor formulation, chemistry, and documentation so your results stay consistent across runs and re-orders.
- Format options: solid or pre-dissolved solution (choose solvent), target concentration, aliquots, light/moisture-protected packaging
- Chemistry options: free base/acid vs salt forms, hydrate/solvate preference, stereoisomer control (single enantiomer or racemate), close analogs
- Add-on labels & handles: D/¹³C/¹⁵N isotopes (LC-MS/internal standards), azide/alkyne or other functional handles for conjugation
- QC & documentation: standard COA or enhanced analytical pack (HPLC/LC-MS/NMR), chiral purity, residual solvents, water content (KF), method-specific specs
- Scale & continuity: mg to gram scale, bulk pricing, lot reservation, repeat-order continuity
To quote quickly, tell us: compound name + CAS/structure (SMILES or mol file), intended assay context, solvent preference, salt/stereochemistry requirements, purity/QC level, and the amount (mg–g).
Can’t find the compound you’re looking for?
Send the CAS or structure and your specs. We can help source it, suggest close equivalents, or discuss custom synthesis with the right QC documentation (RUO).
A self-amplifying nerve-fibroblast circuit drives colorectal cancer progression. Cancer Cell 2026 Jul 24:S1535-6108(26)00305-3. PMID: 42497870
Concurrent genetic and non-genetic resistance mechanisms to KRAS inhibition in colorectal cancer. Cancer Cell 2026 May 21:S1535-6108(26)00220-5. PMID: 42167227
The target landscape of clinical kinase drugs. Science 2017 Dec 1;358(6367):eaan4368.
Galectin 3-binding protein (LGALS3BP) depletion attenuates hepatic fibrosis by reducing transforming growth factor-β1 (TGF-β1) availability and inhibits hepatocarcinogenesis. Cancer Commun (Lond) 2024 Oct;44(10):1106-1129. PMID: 39073023
Nanoporous titanium implant surface promotes osteogenesis by suppressing osteoclastogenesis via integrin β1/FAKpY397/MAPK pathway. Bioact Mater 2021 Jul 1:8:109-123. PMID: 34541390
Matrix stiffness modulates tip cell formation through the p-PXN-Rac1-YAP signaling axis. Bioact Mater 2021 Jun 1:7:364-376. PMID: 34466738
Netrin-1 Promotes Pancreatic Tumorigenesis and Innervation through NEO1. Cancer Res 2025 Dec 31. PMID: 41474982
Fibronectin-induced overactivation of αβ-PI3K-PIP3-PDK1-ILK signaling drives aortic disease in Marfan syndrome. Nat Commun 2026 Jul 6;17(1):5631. PMID: 42409814
Human iPSC-based Modeling of Pulmonary Fibrosis Reveals p300/CBP Inhibition Suppresses Alveolar Transitional Cell State. Nat Commun 2026 Feb 12;17(1):1214. PMID: 41680175
Biomimetic organo-hydrogels reveal the adipose tissue local mechanical anisotropy regulates ovarian cancer invasion. Nat Commun 2025 Sep 29;16(1):8541. PMID: 41022685
