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Chemical Structure| 1061353-68-1 Chemical Structure| 1061353-68-1

Structure of PND-1186
CAS No.: 1061353-68-1

Chemical Structure| 1061353-68-1

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PND-1186 is a potent FAK inhibitor with IC50 of 1.5 nM.

Synonyms: VS-4718; SR-2516; SR-2156

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Product Details of PND-1186

CAS No. :1061353-68-1
Formula : C25H26F3N5O3
M.W : 501.50
SMILES Code : O=C(NC)C1=CC=CC=C1NC2=CC(NC3=CC=C(N4CCOCC4)C=C3OC)=NC=C2C(F)(F)F
Synonyms :
VS-4718; SR-2516; SR-2156
MDL No. :MFCD28125506
InChI Key :IGUBBWJDMLCRIK-UHFFFAOYSA-N
Pubchem ID :25073775

Safety of PND-1186

GHS Pictogram:
Signal Word:Warning
Hazard Statements:H302-H315-H319-H335
Precautionary Statements:P261-P305+P351+P338

Related Pathways of PND-1186

RTK
cytoskeleton

Isoform Comparison

Biological Activity

Target
  • FAK

    FAK, IC50:1.5 nM

In Vitro:

Cell Line
Concentration Treated Time Description References
KP cells 1 µM To investigate the effect of FAK inhibitor on KP cell proliferation, the results showed that FAK inhibitor significantly inhibited KP cell proliferation. PMC7167297
KI cells 5 ng/mL 1 hour To investigate the effect of TGF-β on pSTAT3 and pSMAD3 signaling in KI cells, the results showed that TGF-β significantly inhibited pSTAT3 expression. PMC7167297
Panc-1 cells 5 ng/mL 1 hour To investigate the effect of TGF-β on pSTAT3 and pSMAD3 signaling in Panc-1 cells, the results showed that TGF-β significantly inhibited pSTAT3 expression. PMC7167297
HepG2 cells 0.5 μM and 1 μM 48 hours To evaluate the effect of PND-1186 on HCC cell proliferation and apoptosis, results showed that PND-1186 significantly inhibited cell proliferation and induced G0/G1 phase arrest and apoptosis. PMC5423113
Huh7.5 cells 0.5 μM and 1 μM 48 hours To evaluate the effect of PND-1186 on HCC cell proliferation and apoptosis, results showed that PND-1186 significantly inhibited cell proliferation and induced G0/G1 phase arrest and apoptosis. PMC5423113
HepG2 cells 7.1 μM 48 hours PND1186 reduced the viability of HepG2 cells with an IC50 value of 7.1 μM. PMC8597092
Huh7 cells 10 μM 48 hours PND1186 reduced the viability of Huh7 cells with an IC50 value of 10 μM. PMC8597092
HEY cells 0.1 μM 72 hours promoted G0/G1 cell cycle arrest followed by cell death PMC4126870
OVCAR8 cells 0.1 μM 72 hours promoted G0/G1 cell cycle arrest followed by cell death PMC4126870
SKOV3-IP cells 1.0 μM 72 hours remained resistant to VS-4718 treatment PMC4126870
OVCAR10 cells 1.0 μM 72 hours remained resistant to VS-4718 treatment PMC4126870

In Vivo:

Species
Animal Model
Administration Dosage Frequency Description References
Mice KPC mouse model Oral 20 mg/kg/day daily for 35 days FAK inhibitor significantly extended survival in KPC mice and reduced tumor fibrosis and immunosuppressive cell populations. PMC4935930
Mice SCC tumor model Oral 50 mg/kg Twice a day for 1.5 months Investigated the immunomodulatory effects of VS-4718 on SCC tumors, finding that VS-4718 reduced Tregs within the tumor, promoting a CD8+ T cell-mediated anti-tumor response and leading to tumor regression. PMC4597190
mice KPC mouse model oral 25 mg/kg Once daily for 12 days To investigate the effect of FAK inhibitor on tumor growth in the KPC mouse model, the results showed that FAK inhibitor significantly inhibited tumor growth. PMC7167297
Mice Xenograft model Intramuscular and intrahepatic injection 3 mg/kg trametinib, 300 μg ganitumab trametinib once daily, 5 days/week; ganitumab twice weekly for 28 days To evaluate the effect of FAK silencing on HCC tumor growth, results showed that FAK silencing significantly inhibited tumor growth. PMC5423113
nude mice HEY cell xenograft model subcutaneous injection 40 mg/kg daily for 3 days FAK inhibition or β5 knockdown reduced HEY cell growth under anchorage-independent conditions with corresponding decreases in orthotopic tumor growth PMC4126870

Clinical Trial:

NCT Number Conditions Phases Recruitment Completion Date Locations
NCT01849744 Non Hematologic Cancers|Metast... More >>atic Cancer Less << PHASE1 TERMINATED 2025-06-17 HonorHealth Research Institute... More >>, Scottsdale, Arizona, 85258, United States|Samuel Oschin Comprehensive Cancer Institute, Cedars-Sinai Medical Center, Los Angeles, California, 90048, United States|Florida Cancer Specialists, Sarasota, Florida, 34232, United States|Washington University School of Medicine, Division of Oncology, Saint Louis, Missouri, 63110, United States|Sarah Cannon Research Institute, Nashville, Tennessee, 37203, United States Less <<
NCT02215629 Relapsed or Refractory Acute M... More >>yeloid Leukemia|Relapsed or Refractory B-Cell Acute Lymphoblastic Leukemia Less << PHASE1 WITHDRAWN 2025-11-16 -

Protocol

Bio Calculators
Preparing Stock Solutions 1mg 5mg 10mg

1 mM

5 mM

10 mM

1.99mL

0.40mL

0.20mL

9.97mL

1.99mL

1.00mL

19.94mL

3.99mL

1.99mL

Dissolving Methods
Please choose the appropriate dissolution scheme according to your animal administration guide.For the following dissolution schemes, clear stock solution should be prepared according to in vitro experiments, and then cosolvent should be added in turn:

in order to ensure the reliability of the experimental results, the clarified stock solution can be properly preserved according to the storage conditions; The working fluid for in vivo experiment is recommended to be prepared now and used on the same day;

The percentage shown in front of the following solvent refers to the volume ratio of the solvent in the final solution; If precipitation or precipitation occurs in the preparation process, it can be assisted by heating and/or ultrasound.
Protocol 1
Protocol 2
 

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