ArticleCancer biology & therapy2010
Oral delivery of PND-1186 FAK inhibitor decreases tumor growth and spontaneous breast to lung metastasis in pre-clinical models.
Article in Cancer biology & therapy, 2010. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 80 papers.
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Who cites it
80 citing papers in PubMed, 124 citations in OpenAlex.
- Randomized, Open-Label, Crossover Studies Evaluating the Effect of Food and Liquid Formulation on the Pharmacokinetics of the Novel Focal Adhesion Kinase (FAK) Inhibitor BI 853520.Targeted oncology · 2019Trial
- Cytoskeletal dynamics in breast cancer: mechanistic insights and therapeutic opportunities.Journal of the National Cancer Center · 2026Review
- Disarming cancer resistance: FAK as a therapeutic target.Trends in cancer · 2026Review
- Targeting the hydrophobic pockets of FAK/PYK2 FAT domain: a highly effective inhibitory strategy suppressing tumor growth and eliminating metastasis.Cell communication and signaling : CCS · 2025Article
- Self-emulsifying Nano-PND oral delivery systems of PND1186: In silico modeling for bioavailability estimation.Journal of molecular liquids · 2025Article
- Identification of potential FAK inhibitors using mol2vec molecular descriptor-based QSAR, molecular docking, ADMET study, and molecular dynamics simulation.Molecular diversity · 2024Article
- The Role of SCARA5 as a Potential Biomarker in Squamous Cell Carcinoma of the Lung.International journal of molecular sciences · 2024Article
- High-throughput chemogenetic drug screening reveals PKC-RhoA/PKN as a targetable signaling vulnerability in GNAQ-driven uveal melanoma.Cell reports. Medicine · 2023Article
- Focal adhesion kinase: from biological functions to therapeutic strategies.Experimental hematology & oncology · 2023Review
- SCARA5 Is Overexpressed in Prostate Cancer and Linked to Poor Prognosis.Diagnostics (Basel, Switzerland) · 2023Article
- THSD7A Positivity Predicts Poor Survival and Is Linked to High FAK Expression and FGFR1-Wildtype in Female Patients with Squamous Cell Carcinoma of the Lung.International journal of molecular sciences · 2023Article
- VE-Cadherin modulates β-catenin/TCF-4 to enhance Vasculogenic Mimicry.Cell death & disease · 2023Article
- THSD7A Positivity Is Associated with High Expression of FAK in Prostate Cancer.Diagnostics (Basel, Switzerland) · 2023Article
- Immunoglobulin superfamily 9 (IGSF9) is trans-activated by p53, inhibits breast cancer metastasis via FAK.Oncogene · 2022Article
- Article
- Matrix stiffening and acquired resistance to chemotherapy: concepts and clinical significance.British journal of cancer · 2022Review
- Focal adhesion kinase inhibitors, a heavy punch to cancer.Discover oncology · 2021Review
- FAK inhibitors as promising anticancer targets: present and future directions.Future medicinal chemistry · 2021Review
- Discovery of Novel 2,4-Dianilinopyrimidine Derivatives Containing 4-(Morpholinomethyl)phenyl andMolecules (Basel, Switzerland) · 2021Article
- FAK inhibition alone or in combination with adjuvant therapies reduces cancer stem cell activity.NPJ breast cancer · 2021Article
20 more citing papers are in PubMed but not listed here.
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Authors and funding
12 authors at 1 institution in 1 country.
Funding
Abstract
Tumor metastasis is a leading cause of cancer-related death. Focal adhesion kinase (FAK) is a cytoplasmic tyrosine kinase recruited to integrin-mediated matrix attachment sites where FAK activity is implicated in the control of cell survival, migration, and invasion. Although genetic studies support the importance of FAK activity in promoting tumor progression, it remains unclear whether pharmacological FAK inhibition prevents tumor metastasis. Here, we show that the FAK inhibitor PND-1186 blocks FAK Tyr-397 phosphorylation in vivo and exhibits anti-tumor efficacy in orthotopic breast carcinoma mouse tumor models. PND-1186 (100 mg/kg intraperitoneal, i.p.) showed promising pharmacokinetics (PK) and inhibited tumor FAK Tyr-397 phosphorylation for 12 hours. Oral administration of 150 mg/kg PND-1186 gave a more sustained PK profile verses i.p., and when given twice daily, PND-1186 significantly inhibited sygeneic murine 4T1 orthotopic breast carcinoma tumor growth and spontaneous metastasis to lungs. Moreover, low-level 0.5 mg/ml PND-1186 ad libitum administration in drinking water prevented oncogenic KRAS- and BRAF-stimulated MDA-MB-231 breast carcinoma tumor growth and metastasis with inhibition of tumoral FAK and p130Cas phosphorylation. Although PND-1186 was not cytotoxic to cells in adherent culture, tumors from animals receiving PND-1186 exhibited increased TUNEL staining, decreased leukocyte infiltrate and reduced tumor-associated splenomegaly. In vitro, PND-1186 reduced tumor necrosis factor-a triggered interleukin-6 cytokine expression, indicating that FAK inhibition may impact tumor progression via effects on both tumor and stromal cells. As oral administration of PND-1186 also decreased experimental tumor metastasis, PND-1186 may therefore be useful clinically to curb breast tumor progression.
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Registered trials
Read under generation 80e0d062 · epoch 390. Bibliography from PubMed, PubMed Central and OpenAlex; grants from NIH RePORTER; trial links from ClinicalTrials.gov; estimates, votes and beliefs from the OpenQuestion graph.