FNIII14
Based on 1 Customer Validation
FNIII14 is a β1-integrin inhibitory peptide. FNIII14 induces the conformational shift of β1-integrin from the active form to the inactive form, blocks integrin-mediated signaling pathways, disrupts the interaction between VLA-4 and fibronectin, inhibits the phosphorylation of FAK/Akt, suppresses cell adhesion, fibronectin fibril formation and chondrocyte proliferation, induces chondrocyte apoptosis and cartilage degeneration, upregulates the pro-apoptotic protein Bim, and binds to membrane-bound eEF1A. FNIII14 reversibly disrupts cell adhesion without reducing cell viability, accelerates adipocyte differentiation, and loosens tumor matrix architecture to enhance the permeability of nanotherapeutic agents. FNIII14 can be used in research related to neuroblastoma, pancreatic cancer, acute myeloid leukemia, colitis-associated colorectal cancer, osteoarthritis, and atherosclerosis.
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- Pureza: 96.55%
- No. CAS: 206536-96-1
- Fòrmula: C103H163N21O35
- Peso molecular:2255.52
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Almacenamiento:
Sealed storage, away from moisture.
Powder -80°C, 2 years , -20°C, 1 year* In solvent : -80°C, 6 months; -20°C, 1 month (sealed storage, away from moisture)
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Actividad biológica
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Chemical Information
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Solvente y solubilidad
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Actividad biológica
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β1-integrin |
Akt |
FAK |
Bim |
eEF1A |
FNIII14 potently inhibits A375SM human melanoma cell adhesion to FN substrate by inducing a conformational change in β1-integrin from the active to the inactive form, with the YTIYVIAL sequence required for activity[1].
FNIII14 inhibits aggressive properties and anoikis resistance of T98G, 9L, and U251 glioblastoma cells, and sensitizes these cells to Temozolomide (HY-17364) by down-regulating MGMT, exerting potent anti-cancer effects via β1-integrin inactivation[1].
FNIII14 inhibits malignant properties of IMR-32 human neuroblastoma cells and MIA-PaCa 2 human pancreatic carcinoma cells by inducing proteasomal degradation of N-Myc and c-myc, respectively, via β1-integrin inactivation[1].
FNIII14 reverses cell adhesion-mediated drug resistance to Ara C (Cytarabine) (HY-13605) in U937 and HL-60 leukemia cells, and enhances chemosensitivity to 5-FU (5-Fluorouracil) (HY-90006) in Ca9-22/FR2 OSCC cells via β1-integrin inactivation[1].
FNIII14 (100 μg/mL; 2 h pre-incubation plus 24 h co-incubation with 1×10-6 M Ara C) restores sensitivity to Ara C and overcomes cell adhesion-mediated drug resistance in U937 cells and HL-60 cells[2].
FNIII14 (100 μg/mL; 2 h pre-incubation, 6 h co-incubation with 1×10-6 M cytosine arabinoside, 18 h co-incubation with 1×10-6 M cytosine arabinoside, 2 h incubation alone) inhibits the FN-induced FAK/Akt/Bcl-2 signaling pathway in U937 cells, suppressing FAK phosphorylation alone and enhancing cytosine Ara C-mediated suppression of Akt phosphorylation and Bcl-2 expression[2].
FNIII14 (50 μg/mL; 45 min) inactivates β1-integrin on human melanoma Mum2B cells[3].
FNIII14 (50 μg/mL; 6 h) functional blocking reduces the in vitro migration of human melanoma Mum2B cells to levels similar to poorly invasive Mum2C cells[3].
FNIII14 (50 μg/mL; 6 h) functional blocking significantly reduces the in vitro migration of mouse breast cancer 4T1 cells[3].
FNIII14 (12.5 μg/mL; 6 h) functional blocking abrogates the enhanced in vitro invasion of eEF1A-overexpressing human melanoma Mum2B cells[3].
FNIII14 (25 µg/mL; 3 days) functionally inactivates β1-integrins in human glioblastoma T98G cells, rat gliosarcoma 9L cells, and mouse glioma GL261 cells, suppressing malignant cell behaviors and potentiating temozolomide cytotoxicity with 25 µg/mL FNIII14 incubated for 3 days alongside 125 mM temozolomide in GL261 cells[4].
FNIII14 suppresses cell survival and proliferation in human glioblastoma T98G cells, rat gliosarcoma 9L cells, and human neuroblastoma IMR-32 cells, and reduces N-myc levels via proteasomal degradation in human neuroblastoma IMR-32, NB-1, and KELLY cells[4].
FNIII14 inhibits disseminative migration in human glioblastoma T98G cells and murine T lymphoma L5178Y-ML25 cells[4].
FNIII14 potentiates the cytotoxicity of multiple chemotherapeutic agents in human glioblastoma T98G cells, rat gliosarcoma 9L cells, mouse mammary tumor 4T1 cells, mouse melanoma B16BL6 cells, and 5-FU-resistant oral squamous cell carcinoma Ca9-22/FR2 cells[4].
FNIII14 disrupts cell adhesion-mediated drug resistance to cytosine Ara C in human acute myelogenous leukemia U937 cells and HL-60 cells[4].
FNIII14 (10-10-10-6 M anthracycline chemotherapeutic agent co-administered; 24 h) synergistically enhances the cytotoxicity of anthracycline chemotherapeutic agent in mouse mammary tumor 4T1 cells, reducing the anthracycline chemotherapeutic agent IC50 to 0.32 nM with CI values <1[6].
FNIII14 (10-10-10-6 M anthracycline antibiotic co-administered; 24 h) synergistically enhances the cytotoxicity of anthracycline antibiotic and a broad range of other anti-cancer drugs in mouse melanoma B16BL6 cells, reducing the anthracycline antibiotic IC50 to 0.005 nM with CI values <1[6].
FNIII14 (50-100 μg/mL; 1 h preincubation, followed by adhesion incubation) reversibly inhibits integrin α4β1-mediated adhesion of human Burkitt’s lymphoma Ramos cells to fibronectin substrate and TNF-α-stimulated HUVEC monolayers in a dose-dependent manner, with no impact on cell viability[7].
FNIII14 (22-44 μM; 1 h preincubation followed by 1 h adhesion incubation) inhibits integrin αvβ3-mediated adhesion of murine T lymphoma L5178Y-ML25 cells to vitronectin substrate in a dose-dependent manner without affecting nonspecific adhesion to poly-L-Lys[7].
FNIII14 (50-100 μg/mL; 1 h preincubation followed by 2 h migration incubation) inhibits vitronectin-induced, integrin αvβ3-mediated migration of murine T lymphoma L5178Y-ML25 cells in a dose-dependent manner[7].
FNIII14 (200 μg/mL; 20 min) down-regulates vitronectin-stimulated tyrosine phosphorylation of p125FAK and paxillin in murine T lymphoma L5178Y-ML25 cells, and this effect is reversed by the protein tyrosine phosphatase inhibitor Phenylarsine Oxide (HY-131901)[7].
FNIII14 accelerates insulin-induced adipocyte differentiation of mouse preadipocyte ST-13 cells by inactivating β1-integrin and reducing cell adhesion to FN substrate[1].
FNIII14 suppresses the myofibroblastic conversion of rat hepatic stellate cells by inhibiting integrin-mediated adhesive interactions, blocking phenotypic activation of freshly isolated cells and matrix assembly by activated cells[1].
FNIII14 binds specifically to membrane-type eEF1A (p50) on human melanoma Mum2B, human melanoma Mum2C, and mouse breast cancer 4T1 cells, but not on human breast cancer MCF-7 cells[3].
FNIII14 inactivates β1-integrins in fibroblasts, inhibiting TNIIIA2-stimulated fibroblast-mediated proliferation of preneoplastic epithelial cells[4].
FNIII14 (10 µg/mL; 24 h) reduces β1 integrin activity in primary human OA chondrocytes, as shown by decreased immunofluorescence staining intensity[5].
FNIII14 (10 µg/mL; 24 h) reduces β1 integrin activity in primary human OA chondrocytes, as measured by flow cytometry[5].
FNIII14 (1-20 µg/mL; 7 day) inhibits proliferation of primary human OA chondrocytes in a dose-dependent manner, with the strongest effect at 20 µg/mL[5].
FNIII14 (10 µg/mL; 24 h) increases ERK1/2 phosphorylation and decreases SOX9 protein expression in primary human OA chondrocytes, with ERK1/2 phosphorylation elevated transiently from 30 minutes to 24 hours post-treatment[5].
FNIII14 (12 h) is released from PMNPs in a FAP-α-dependent manner, with over 70% of the peptide liberated after 12 h of FAP-α exposure[8].
FNIII14 inhibits ACC-derived CAF function by reducing p-ITGB1 expression by 49%, and decreasing downstream stromal products α-SMA and COL1A1[8].
FNIII14 (50-100 µg/mL; 10 days) dose-dependently accelerates insulin-induced adipocyte differentiation of ST-13 cells, with 100 µg/mL increasing adipocyte numbers by 7-10-fold and glycerophosphate dehydrogenase activity by 7-8-fold, while suppressing fibronectin incorporation into insoluble pool II fibrils[10].
FNIII14 (0-100 µg/mL; 2 days) dose-dependently inhibits fibronectin matrix assembly in ST-13 cells, with 50 µg/mL achieving near-total suppression of fibronectin incorporation into insoluble pool II fibrils[10].
FNIII14 (0-100 µg/mL; 60-80 minutes) dose-dependently inhibits α5β1-mediated adhesion of ST-13 cells to fibronectin and reverses β1 integrin-activated adhesion, with 100 µg/mL producing maximal suppression[10].
FNIII14 (100 µg/mL; 30 minutes) induces a conformation change of β1 integrins on K562 cells from active to resting state, inhibiting Mn2+-activated integrin activity[10].
FNIII14 (0-100 µg/mL; 30 minutes) dose-dependently dissociates the binding of the 110 kDa fibronectin fragment to ST-13 cells and binds to ST-13 cells directly, with 100 µg/mL producing maximal displacement of the fibronectin fragment[10].
FNIII14 (10 µg/mL; 24 h) induces apoptosis in primary human OA chondrocytes, increasing both early and late apoptosis rates compared to untreated cells[5].
FNIII14 (1-10 µg/mL; 6-24 h) induces apoptosis in primary human OA chondrocytes after 6-24 hours of incubation, with a significant increase in TUNEL-positive cells observed at 10 µg/mL for 24 hours[5].
FNIII14 (1-3 h) upregulates the expression of pro-apoptotic Bim splice variants (BimEL, BimL, BimS) in mouse mammary tumor 4T1 cells, with a synergistic increase when co-administered with Doxorubicin (HY-15142A)[6].
FNIII14 induces the release of pro-apoptotic Bim from microtubules and promotes its translocation to mitochondria in mouse mammary tumor MMT cells[6].
FNIII14 (6 h) promotes the release of BimEL from tubulin polymers into the soluble low-density fraction in mouse mammary tumor MMT cells, associated with tubulin depolymerization[6].
FNIII14 (3-6 h) promotes the binding of pro-apoptotic Bim to anti-apoptotic Bcl-2 in mouse mammary tumor MMT cells[6].
FNIII14 (10 µg/mL; 24 h) dysregulates gene expression in primary human OA chondrocytes, reducing cartilage-specific marker and anabolic factor expression while increasing inflammatory cytokine expression[5].
FNIII14 (10-10-10-6 M doxorubicin co-administered; 24 h post 24 h siRNA transfection) has its synergistic enhancement of doxorubicin cytotoxicity in mouse mammary tumor 4T1 cells completely abrogated by Bim knockdown, with CI values shifting to 1.07[6].
FNIII14 (3-24 h) potently suppresses pTNIIIA2-mediated pro-atherosclerotic phenotypes in RAW 264.7 cells, including upregulated LOX1 expression, downregulated ABCA1 and ABCG1 expression, increased phagocytic activity, and excessive intracellular lipid accumulation[9].
MedChemExpress (MCE) has not independently confirmed the accuracy of these methods. They are for reference only.
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Cell Line:U937, HL-60
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Concentration:100 μg/mL
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Incubation Time:2 h pre-incubation; 24 h co-incubation with 1×10-6 M Ara C
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Result:Eliminated the viability difference between FN- and BSA-adhered cells treated with Ara C, restoring chemosensitivity to levels seen in BSA-adhered cells in U937 and HL-60 cells.
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Cell Line:U937
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Concentration:100 μg/mL
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Incubation Time:2 h pre-incubation; 6 h co-incubation with 1×10-6 M cytosine arabinoside (Akt analysis); 18 h co-incubation with 1×10-6 M cytosine arabinoside (Bcl-2 analysis); 2 h incubation alone (FAK analysis)
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Result:Almost completely suppressed FN-induced FAK (Tyr397) phosphorylation.
Further suppressed FN-induced Akt (Ser473) phosphorylation compared to cytosine arabinoside alone; combined treatment with cytosine arabinoside resulted in near-complete suppression of phosphorylated Akt.
Further suppressed FN-induced Bcl-2 expression compared to cytosine arabinoside alone; combined treatment with cytosine arabinoside resulted in near-complete suppression of Bcl-2 expression.
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Cell Line:human melanoma Mum2B cells
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Concentration:50 μg/mL
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Incubation Time:6 h
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Result:Reduced cell migration distance to ~10% of the control IgG-treated group, matching the low migration level of poorly invasive Mum2C cells.
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Cell Line:human melanoma Mum2B cells
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Concentration:50 μg/mL
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Incubation Time:6 h
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Result:Reduced the number of invaded cells to ~25% of the control IgG-treated group, matching the low invasion level of poorly invasive Mum2C cells.
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Cell Line:mouse breast cancer 4T1 cells
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Concentration:50 μg/mL
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Incubation Time:6 h
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Result:Reduced cell migration to ~58% of the control IgG-treated group.
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Cell Line:mouse breast cancer 4T1 cells
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Concentration:50 μg/mL
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Incubation Time:24 h
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Result:Reduced the number of invaded cells to ~53% of the control IgG-treated group.
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Cell Line:eEF1A-overexpressing human melanoma Mum2B cells
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Concentration:12.5 μg/mL
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Incubation Time:6 h
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Result:Reduced the ~3.5-fold increase in invasion caused by eEF1A overexpression to levels similar to untransfected control cells.
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Cell Line:mouse mammary tumor 4T1 cells
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Concentration:10-10-10-6 M (anthracycline chemotherapeutic agent; co-administered with FNIII14)
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Incubation Time:24 h
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Result:Dramatically reduced 4T1 cell viability compared to treatment with anthracycline chemotherapeutic agent and control FNIII14scr.
Produced a combination index (CI) of 0.86 at 10-7 M anthracycline chemotherapeutic agent and 0.89 at 10-8 M anthracycline chemotherapeutic agent, indicating a synergistic effect.
Reduced the IC50 of anthracycline chemotherapeutic agent in 4T1 cells to 0.32 nM, compared to 250 nM in FNIII14scr-treated cells.
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Cell Line:mouse melanoma B16BL6 cells
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Concentration:10-10-10-6 M (anthracycline antibiotic; co-administered with FNIII14)
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Incubation Time:24 h
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Result:Dramatically reduced B16BL6 cell viability compared to treatment with anthracycline antibiotic and control FNIII14scr.
Produced a combination index (CI) of 0.33 at 10-7 M anthracycline antibiotic and 0.65 at 10-8 M anthracycline antibiotic, indicating a synergistic effect.
Reduced the IC50 of anthracycline antibiotic in B16BL6 cells to 0.005 nM, compared to 100 nM in FNIII14scr-treated cells.
Enhanced the cytotoxicity of multiple other anti-cancer drugs in B16BL6 cells, reducing their IC50 values: actinomycin-type antibiotic (from 10 nM to 0.05 nM), mitomycin-type antibiotic (from 10 nM to 0.025 nM), glycopeptide antibiotic (from 10 nM to 0.02 nM), vinca alkaloid (from 10 nM to 0.001 nM), vinca alkaloid (from 50 nM to 0.01 nM), vinca alkaloid (from 1000 nM to 0.1 nM), purine antimetabolite (from 1000 nM to 5 nM), pyrimidine antimetabolite (from 10 nM to 0.05 nM), and alkylating agent (from 100 nM to 1 nM).
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Cell Line:Bim-silenced mouse mammary tumor 4T1 cells
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Concentration:10-10-10-6 M (doxorubicin; co-administered with FNIII14)
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Incubation Time:24 h (post 24 h siRNA transfection)
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Result:In Bim-silenced cells co-treated with FNIII14 and doxorubicin, produced a combination index (CI) of 1.07 at 10-7 M and 10-8 M doxorubicin, indicating an additive rather than synergistic effect.
In control siRNA-transfected cells, produced a CI of 0.76 at 10-7 M doxorubicin and 0.73 at 10-8 M doxorubicin, maintaining the synergistic effect.
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Cell Line:murine T lymphoma L5178Y-ML25 cells
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Concentration:50-100 μg/mL
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Incubation Time:1 h preincubation followed by 2 h migration incubation
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Result:Inhibited vitronectin-induced, integrin αvβ3-mediated migration of L5178Y-ML25 cells in a dose-dependent manner at 50 μg/mL and 100 μg/mL compared to the control IgG group.
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Cell Line:murine T lymphoma L5178Y-ML25 cells
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Concentration:100 μg/mL
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Incubation Time:20 min
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Result:Abrogated vitronectin-stimulated tyrosine phosphorylation of p125FAK and paxillin, keeping phosphorylation at basal levels.
Had inhibitory effect on cell adhesion to vitronectin reversed by phenylarsine oxide, which also restored reduced tyrosine phosphorylation of p125FAK and paxillin.
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Cell Line:murine T lymphoma L5178Y-ML25 cells
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Concentration:200 μg/mL
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Incubation Time:20 min
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Result:Inhibited vitronectin-stimulated tyrosine phosphorylation of p125FAK and paxillin.
Had inhibitory effect on cell adhesion to vitronectin reversed by phenylarsine oxide, which also restored reduced tyrosine phosphorylation of p125FAK and paxillin.
FNIII14 (200 μg/mouse; i.p.; daily on days 0 to 10) coadministered with 200 μg/mouse of another agent (i.p.; single dose on day 4) strongly suppresses mammary carcinoma metastasis in BALB/c mice without altering body weight or primary tumor size[6].
FNIII14 (50-700 μg/mouse; i.v.; single coinjection with tumor cells) potently inhibits liver and spleen metastases of L5178Y-ML25 lymphoma cells in CDF1 mice, achieving 80-99% inhibition of organ weight increases at doses as low as 22 nmol (50 μg/mouse)[7].
FNIII14 (1 mg; i.v.; single dose) does not augment the myelosuppressive effects of Ara C (20 mg; i.p.; two doses: first on day 0, second 12 hours after the first dose) in healthy C57BL/6 Cr Slc mice[2].
FNIII14 (0.1-1 µg; o.a.; single injection) induces significant cartilage degeneration in BALB/c mice at 12 weeks post-administration, with minimal to no synovitis[5].
FNIII14 (100 µg/head; i.v.; every other day; 9 weeks) potently suppresses atherosclerotic plaque formation in LDLR−/− mice, reducing lesion area by approximately 40% relative to controls[9].
FNIII14 (starting 10 days post-implantation) is required for hematogenous and lymphatic metastasis of Mum2B melanoma xenografts in KSN/SLC nude mice, and masking FNIII14 completely blocks this metastasis without altering primary tumor growth[3].
FNIII14 (starting 8 days post-implantation) is required for spontaneous lung metastasis of 4T1 breast cancer xenografts in BALB/c mice, and masking FNIII14 significantly suppresses this metastasis[3].
MedChemExpress (MCE) has not independently confirmed the accuracy of these methods. They are for reference only.
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Animal Model:CB-17/lcrCrj-scid/scid severe combined immunodeficiency (SCID) (6 weeks old, irradiated at 4 Gy, injected with 5×106 U937 cells intravenously to establish minimal residual disease)[2]
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Dosage:1 mg (FNIII14); 20 mg (cytarabine)
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Administration:i.v. (single dose on day 7 post-transplantation; FNIII14); i.p. (single dose on day 7 post-transplantation; cytarabine)
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Result:Achieved 100% survival of mice through the 62-day observation period.
Rendered bone marrow from surviving mice negative for the human Alu sequence, indicating eradication of minimal residual disease.
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Animal Model:C57BL/6 Cr Slc (6 weeks old)[2]
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Dosage:1 mg (FNIII14); 20 mg (Ara C)
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Administration:i.v. (single dose; FNIII14); i.p. (two doses: first on day 0, second 12 hours after the first dose; Ara C)
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Result:Produced nearly identical patterns of white blood cell, neutrophil, lymphocyte, and platelet suppression compared to mice treated with Ara C alone.
Resulted in similar transient suppression (days 1-6) and trough levels of these blood cell types compared to mice treated with Ara C alone.
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Animal Model:BALB/c (8-week-old male, ~22 g)[5]
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Dosage:0.1 µg; 1 µg
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Administration:o.a.; single injection
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Result:Exhibited significantly higher Mankin scores compared to untreated normal mice (p = 0.032), and showed a non-significant trend toward higher scores compared to PBS-injected control mice (p = 0.09) at 0.1 µg dose.
Exhibited significantly higher Mankin scores compared to both untreated normal mice (p = 0.017) and PBS-injected control mice (p = 0.028) at 1 µg dose.
Caused weaker Saf-O staining compared to normal and PBS control groups at both doses.
Induced slight cartilage surface distortion at 0.1 µg dose.
Induced marked surface irregularity, severe structural disruption, and sparse chondrocyte distribution with reduced cellularity at 1 µg dose.
Showed no significant differences in synovitis scores compared to control groups at both doses.
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Animal Model:BALB/c (female, 5 weeks old, mammary carcinoma model via subcutaneous transplantation of minced 4T1 tumor tissue)[6]
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Dosage:200 μg/mouse (FNIII14); 200 μg/mouse (coadministered agent)
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Administration:i.p.; daily on days 0 to 10 (FNIII14); i.p.; single dose on day 4 (coadministered agent)
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Result:Reduced liver weight to ~70% of healthy control levels, compared to ~150% in vehicle-treated tumor-bearing mice.
Reduced liver metastatic tumor burden to near-undetectable levels.
Suppressed metastasis-induced increases in lung and spleen weight.
Reduced lung metastatic tumor burden.
Showed no differences in body weight or primary tumor size compared to other treatment groups.
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Animal Model:CDF1 mice (6 weeks old; 5 mice per group; lymphoma metastasis model via i.v. injection of murine T lymphoma L5178Y-ML25 cells)[7]
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Dosage:50 μg/mouse; 200 μg/mouse; 700 μg/mouse
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Administration:i.v.; single coinjection with tumor cells
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Result:Inhibited liver weight increase by 97-99% and spleen weight increase by 100-112% at 700 μg/mouse, with no detectable metastatic foci in liver or spleen sections.
Strongly prevented liver and spleen metastases at 200 μg/mouse.
Inhibited liver weight increase by 80% and spleen weight increase by 84% at 50 μg/mouse.
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Animal Model:LDLR−/− (male, 12 weeks at start of intervention, Western diet-induced atherosclerosis)[9]
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Dosage:100 µg/head
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Administration:i.v.; every other day; 9 weeks
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Result:Reduced atherosclerotic lesion size by approximately 40% (measured as Sudan red-positive area relative to total aortic area) compared to controls.
Showed no difference in body weight between groups.
Chemical Information
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No. CAS 206536-96-1
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Appearance Solid
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Peso molecular 2255.52
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Fòrmula C103H163N21O35
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Color White to off-white
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Sequence
Thr-Glu-Ala-Thr-Ile-Thr-Gly-Leu-Glu-Pro-Gly-Thr-Glu-Tyr-Thr-Ile-Tyr-Val-Ile-Ala-Leu
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Sequence Shortening
TEATITGLEPGTEYTIYVIAL
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Envío
Room temperature in continental US; may vary elsewhere.
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Almacenamiento
Sealed storage, away from moisture
Powder -80°C 2 years -20°C 1 year * In solvent : -80°C, 6 months; -20°C, 1 month (sealed storage, away from moisture)
Solvente y solubilidad
DMSO : 25 mg/mL (11.08 mM; Need ultrasonic; Hygroscopic DMSO has a significant impact on the solubility of product, please use newly opened DMSO)
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.
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.
Concentration (start) × Volume (start) = Concentration (final) × Volume (final)
Pureza y Documentación
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Ficha de datos (311 KB)
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SDS (254 KB)
- English - EN (254 KB)
- Français - FR (254 KB)
- Deutsch - DE (254 KB)
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- Español - ES (254 KB)
- Swedish - SV (254 KB)
- Italian - IT (254 KB)
- Korean - KR (254 KB)
- Portuguese - PT (254 KB)
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Instrucciones de manejo (2659 KB)
Referencias
[2]. Matsunaga T, et al. Combination therapy of an anticancer drug with the FNIII14 peptide of fibronectin effectively overcomes cell adhesion-mediated drug resistance of acute myelogenous leukemia. Leukemia. 2008 Feb;22(2):353-60. [Content Brief]
[3]. Itagaki K, et al. Exposure of the cryptic de-adhesive site FNIII14 in fibronectin molecule and its binding to membrane-type eEF1A induce migration and invasion of cancer cells via β1-integrin inactivation. American journal of cancer research. 2020;10(11):3990-4004. [Content Brief]
[4]. Fujita M, et al. Involvement of Integrin-Activating Peptides Derived from Tenascin-C in Cancer Aggression and New Anticancer Strategy Using the Fibronectin-Derived Integrin-Inactivating Peptide. Molecules (Basel, Switzerland). 2020 Jul 16;25(14):3239. [Content Brief]
[5]. Nishimura F, et al. Fibronectin Peptide FNIII14 Enhances Progressive Cartilage Degeneration in Osteoarthritis by Inducing Chondrocyte Apoptosis. Current issues in molecular biology. 2026 Jun 04;48(6):594. [Content Brief]
[6]. Iyoda T, et al. Coadministration of the FNIII14 Peptide Synergistically Augments the Anti-Cancer Activity of Chemotherapeutic Drugs by Activating Pro-Apoptotic Bim. PloS one. 2016;11(9):e0162525. [Content Brief]
[7]. Kato R, et al. A new type of antimetastatic peptide derived from fibronectin. Clin Cancer Res. 2002 Jul;8(7):2455-62. [Content Brief]
[8]. Liu Z, et al. FNIII14 Peptide-Enriched Membrane Nanocarrier to Disrupt Stromal Barriers through Reversing CAFs for Augmenting Drug Penetration in Tumors. Nano letters. 2023 Nov 08;23(21):9963-9971. [Content Brief]
[9]. Iyoda T, et al. Bioactive TNIIIA2 Sequence in Tenascin-C Is Responsible for Macrophage Foam Cell Transformation; Potential of FNIII14 Peptide Derived from Fibronectin in Suppression of Atherosclerotic Plaque Formation. International journal of molecular sciences. 2024 Feb 02;25(3):1825. [Content Brief]
[10]. Kamiya S, et al. Fibronectin peptides derived from two distinct regions stimulate adipocyte differentiation by preventing fibronectin matrix assembly. Biochemistry. 2002 Mar 05;41(9):3270-7. [Content Brief]
Complete Stock Solution Preparation Table
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.
| Optional Solvent | Concentration Solvent Mass | 1 mg | 5 mg | 10 mg | 25 mg |
|---|---|---|---|---|---|
| DMSO | 1 mM | 0.4434 mL | 2.2168 mL | 4.4336 mL | 11.0839 mL |
| 5 mM | 0.0887 mL | 0.4434 mL | 0.8867 mL | 2.2168 mL | |
| 10 mM | 0.0443 mL | 0.2217 mL | 0.4434 mL | 1.1084 mL |
FNIII14 Related Classifications
HY-P10984 Related Classifications
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