OS-2966
Based on 1 Customer Validation
OS-2966 is a humanized neutralizing monoclonal antibody (huIgG1κ) targeting human CD29 (β1 integrin/ITGB1). OS-2966 blocks integrin β1 signaling, inhibits tumor cell proliferation, invasion, migration and mesenchymal phenotype, and enhances the efficacy of oncolytic herpes simplex virus-1 (oHSV) and anti-angiogenic therapies. OS-2966 can be used in research related to triple-negative breast cancer, high-grade meningioma, glioblastoma and ovarian cancer.
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- Pureté: 99.62%
- Masse moléculaire:145.5 kDa
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Stockage:
Please store the product under the recommended conditions in the Certificate of Analysis.
To place orders, for customer services and technical support, please contact: MedChemExpress USA
Tel: 609-228-6898 E-mail: [email protected] [email protected]
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Activité biologique
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Chemical Information
- Pureté et documentation
- Références
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Help & FAQs
Activité biologique
Human IgG1 kappa
Human
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CD29 |
OS-2966 (20 μg/mL; 0-24 h) disrupts the c-Met/β1 integrin complex in MDA-MB-231 human triple-negative breast adenocarcinoma cells under the condition of 20 μg/mL with a maximum treatment duration of 24 h[1].
OS-2966 (20 μg/mL; 24 h) reverses the AP21967-induced upregulation of the mesenchymal transcription factors Snail and FOXC2, as well as the AP21967-induced mesenchymal morphological changes, in MDA-MB-231-iDimerize-c-Met-β1 human triple-negative breast adenocarcinoma cells[1].
OS-2966 (20 μg/mL; 24 h) reduces the expression of multiple mesenchymal transcription factors (Snail, FOXC1, FOXC2, Slug, ZEB1, ZEB2) in MDA-MB-231-BO bone-tropic human triple-negative breast adenocarcinoma cells[1].
OS-2966 (0.2-100.0 μg/mL; 3 days) inhibits the viability of NF2 wild-type IOMM-Lee anaplastic meningioma cells seeded on laminin-coated plastic, blocks their adhesion, and induces cell rounding[2].
OS-2966 (50 μg/mL; 3 hours) inhibits the phosphorylation of AKT (Ser473) and ERK1/2 (but not that of FAK (Tyr397)) in NF2-wildtype anaplastic meningioma cells IOMM-Lee grown on laminin-coated plastic culture plates, whereas no changes in this signaling pathway are observed in cells grown on uncoated plastic culture plates[2].
OS-2966 (4 h after oHSV infection) inhibits the migration of macrophages toward both oHSV-infected and uninfected LN229 glioblastoma cells[3].
OS-2966 (10 μg/mL; administered after oHSV treatment, during co-culture with macrophages) enhances oHSV replication in primary GBM30 GBM cells co-cultured with RAW264.7 macrophages[3].
OS-2966 (1-5 mg/mL; 12 h) enables targeted transdermal delivery via fractional laser ablation in full-thickness porcine ear skin. Under effective laser conditions, the maximum skin deposition reaches 3.665 μg/cm2, the local skin retention rate is ≥70%, and transdermal penetration is minimized simultaneously[7].
MedChemExpress (MCE) has not independently confirmed the accuracy of these methods. They are for reference only.
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Cell Line:MDA-MB-231-iDimerize-c-Met-β1 human triple-negative breast adenocarcinoma cells (engineered to induce c-Met/β1 complex formation with AP21967)
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Concentration:20 μg/mL
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Incubation Time:24 h
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Result:Reversed the AP21967-induced upregulation of Snail and FOXC2.
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Cell Line:MDA-MB-231-BO bone-seeking human triple-negative breast adenocarcinoma cells
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Concentration:20 μg/mL
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Incubation Time:24 h
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Result:Significantly reduced the expression of all assessed mesenchymal transcription factors in MDA-MB-231-BO cells.
Twist expression was not detectable in these cells.
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Cell Line:MDA-MB-231-iDimerize-c-Met-β1 human triple-negative breast adenocarcinoma cells (engineered to induce c-Met/β1 complex formation with AP21967)
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Concentration:20 μg/mL
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Incubation Time:24 h
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Result:Reversed the AP21967-induced increase in invasiveness.
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Cell Line:NF2-deficient MN3 patient-derived anaplastic meningioma sphere cells
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Concentration:6.8, 12.5, 25.0, 50.0, 100.0 μg/mL
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Incubation Time:5 days
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Result:Suppressed cell viability by approximately 50% relative to untreated controls.
Showed no apparent dose-response effect across the tested concentrations.
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Cell Line:NF2-wild-type IOMM-Lee anaplastic meningioma cells (on uncoated plastic)
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Concentration:0.2, 0.8, 4.0, 20.0, 100.0 μg/mL
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Incubation Time:4 days
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Result:Had no effect on cell viability at any tested concentration.
Maintained relative viability near 100% across all doses.
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Cell Line:NF2-wild-type IOMM-Lee anaplastic meningioma cells (on laminin-coated plastic)
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Concentration:0.2, 0.8, 4.0, 20.0, 100.0 μg/mL (viability assay); 50 μg/mL (morphology assessment)
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Incubation Time:3 days (viability assay); 3 hours (morphology assessment)
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Result:Suppressed cell viability at all tested concentrations, with significant reductions relative to untreated controls at each dose.
Blocked cell attachment to laminin at 50 μg/mL after 3 hours of exposure.
Induced cell rounding at 50 μg/mL after 3 hours of exposure.
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Cell Line:NF2-deficient MN3 patient-derived anaplastic meningioma sphere cells
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Concentration:50 μg/mL
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Incubation Time:3 hours
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Result:Potently suppressed phosphorylation of FAK at Tyr397.
Suppressed phosphorylation of ERK1/2.
Caused no changes in total FAK, total AKT, or phosphorylation of AKT at Ser473.
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Cell Line:NF2-wild-type IOMM-Lee anaplastic meningioma cells (on uncoated or laminin-coated plastic)
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Concentration:50 μg/mL
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Incubation Time:3 hours
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Result:Had no effect on phosphorylation of FAK (Tyr397), AKT (Ser473), or ERK1/2 in cells on uncoated plastic.
Suppressed phosphorylation of AKT (Ser473) and ERK1/2 in cells on laminin-coated plastic.
Had no effect on phosphorylation of FAK (Tyr397) in cells on laminin-coated plastic.
Detected β1 integrin expression in cells across all conditions.
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Cell Line:NF2-deficient MN8 patient-derived anaplastic meningioma cells
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Concentration:12.5, 25.0, 50.0 μg/mL (viability assay); 50 μg/mL (attachment assay)
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Incubation Time:4 days (viability assay); 48 hours (attachment assay)
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Result:Suppressed cell viability on both uncoated and laminin-coated plastic.
Enhanced inhibitory effect on viability was observed in cells grown on laminin-coated plastic at each tested concentration.
Inhibited cell attachment to laminin at 50 μg/mL after 48 hours of exposure.
OS-2966 (5 mg/kg; i.p.; twice a week) enhances oHSV replication and anti-tumor efficacy in subcutaneous glioblastoma xenografts, with a significant increase in viral total flux and reduced tumor growth[3].
OS-2966 (5 mg/kg; i.p.; 1 day prior to oHSV, then twice a week) enhances oHSV replication and anti-tumor efficacy in orthotopic triple-negative breast cancer xenografts, resulting in a 10.9-fold reduction in tumor volume, 100% response rate, and 50% complete tumor regression by day 21[3].
OS-2966 (5 mg/kg; intratumoral; starting 2 days prior to oHSV, then twice a week; 1 month) enhances oHSV anti-tumor efficacy in intracranial glioblastoma xenografts, resulting in reduced tumor size and improved mouse survival[3].
OS-2966 (10 mg/kg; i.p.; twice weekly with an alternating 3/4-day dose interval) monotherapy significantly reduces ascites volume and exhibits significantly increased nighttime wheel activity compared to cisplatin monotherapy in female Athymic Nude-Foxn1nu mice with intraperitoneal ES-2 ovarian cancer xenografts, while combination therapy with cisplatin (10 mg/kg OS-2966 + 2 mg/kg cisplatin; i.p.; twice weekly with an alternating 3/4-day dose interval) yields significantly improved digital efficacy scores and nighttime wheel activity over OS2966 monotherapy[5].
OS-2966 (1 mg/kg; i.p.; twice weekly; alternating with 1 mg/kg bevacizumab) provides equivalent efficacy to standard-dose bevacizumab for inhibiting subcutaneous bevacizumab-naïve glioblastoma growth[6].
OS-2966 (5-30 mg/kg; i.v.) administered systemically intravenously to nonhuman primates at doses up to 30 mg/kg is well tolerated with only minor, reversible hematological and serum chemistry changes at doses above 5 mg/kg[4].
OS-2966 (1-5 mg/kg; i.p.; twice weekly) significantly inhibits subcutaneous bevacizumab-resistant glioblastoma growth, with 5 mg/kg inducing complete tumor regression in 56% of treated mice[6].
OS-2966 (160 μg total; intratumoral; continuous delivery; 28 days) induces complete regression of orthotopic bevacizumab-resistant glioblastoma, inhibits tumor invasion, and triggers massive tumor cell apoptosis[6].
MedChemExpress (MCE) has not independently confirmed the accuracy of these methods. They are for reference only.
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Animal Model:SCID (7-8-week-old female; orthotopic subdural implantation of patient-derived MN3 anaplastic meningioma cells)[2]
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Dosage:20 mg/kg (survival study); 20 mg/kg (mechanism-of-action studies)
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Administration:i.p.; twice weekly; 6 weeks (survival study); i.p.; two doses over 1 week (mechanism-of-action studies)
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Result:Significantly extended overall survival compared to controls.
Showed a significant decrease in Ki-67 labeling index compared to controls, indicating reduced tumor cell proliferation.
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Animal Model:Athymic nu/nu (female, 4 weeks old, outbred)[3]
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Dosage:5 mg/kg
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Administration:i.p.; twice a week
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Result:Increased viral replication to a total flux of 97146.67 compared to 2303.633 for oHSV + control IgG.
Significantly suppressed tumor growth compared to oHSV + control IgG.
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Animal Model:Athymic nu/nu (female, 4 weeks old, outbred)[3]
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Dosage:5 mg/kg
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Administration:i.p.; 1 day prior to oHSV, then twice a week
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Result:Increased viral replication to a total flux of 311398.3 compared to 89636.5 for oHSV + control IgG (p = 0.0495).
Reduced mean tumor volume to 29.6 mm3 compared to 322.16 mm3 for oHSV + control IgG by day 21, representing a 10.9-fold reduction in tumor growth.
Achieved a 100% response rate, with 50% of mice showing complete tumor regression, and 100% of tumors had increased necrosis.
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Animal Model:Athymic nu/nu (female, 4 weeks old, outbred)[3]
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Dosage:5 mg/kg
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Administration:intratumoral; starting 2 days prior to oHSV, then twice a week; 1 month
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Result:Significantly reduced tumor size compared to oHSV + control IgG.
Significantly improved mouse survival compared to either monotherapy.
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Animal Model:athymic mice (5- to 8-week-old female; subcutaneous xenograft of bevacizumab-resistant BRG3 human glioblastoma cells)[6]
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Dosage:1 mg/kg; 5 mg/kg
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Administration:i.p.; twice weekly
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Result:Reduced subcutaneous tumor volume significantly compared with control IgG-treated mice.
Induced complete tumor regression in 56% (5/9) of mice at 5 mg/kg after 8 weeks of treatment.
Induced tumor cell apoptosis detected on histology, whereas no apoptosis was observed in IgG control-treated tumors.
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Animal Model:athymic mice (5- to 8-week-old female; orthotopic xenograft of bevacizumab-resistant BRG3 human glioblastoma cells)[6]
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Dosage:160 μg total
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Administration:intratumoral; continuous delivery; 28 days
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Result:Induced complete tumor regression in all 3 treated mice.
Triggered massive tumor cell apoptosis detected via TUNEL staining.
Inhibited striatal tumor invasion significantly, shown by reduced number of invading cells per section and reduced invasion distance compared with IgG control-treated mice.
Altered the invasive morphology of tumor cells, reducing cellular processes.
| NCT Number | Sponsor | Condition | Start Date |
Phase
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|---|---|---|---|---|
| NCT01329991 | Plexxikon| | 2011-05 | PHASE1 |
Unconjugated
The product can be reconstituted/diluted with sterile PBS or saline.
ELISA, FACS, Functional assay
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Flow cytometric analysis of 1X106 A549 cells with OS-2966 (HY-P990643, red). Cells were fixed with 4% paraformaldehyde. Then stained with the primary antibody at 1/200 dilution for an hour at 4℃. AF 488-conjugated AffiniPure Goat Anti-Human IgG H&L (HY-P83776) was used as the secondary antibody at 1/1,000 dilution for 30 minutes at 4℃. Human IgG1 kappa (HY-P99001, blue) was used as the isotype control, cells without incubation with primary antibody were used as the unlabeled control (black). -
Immobilized Human integrin alpha 2 beta 1 (ITGA2&ITGB1) heterodimer protein can bind OS-2966. The EC50 for this effect is 1.569 ng/mL.
Chemical Information
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Appearance Liquid
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Masse moléculaire 145.5 kDa
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Color Colorless to light yellow
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Livraison
Shipping with dry ice.
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Formulation
Please refer to the lot-specific COA for specific buffer information.
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Stockage
Please store the product under the recommended conditions in the Certificate of Analysis.
Pureté et documentation
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Fiche technique (281 KB)
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SDS (251 KB)
- English - EN (251 KB)
- Français - FR (251 KB)
- Deutsch - DE (251 KB)
- Norwegian - NO (251 KB)
- Español - ES (251 KB)
- Swedish - SV (251 KB)
- Italian - IT (251 KB)
- Korean - KR (251 KB)
- Portuguese - PT (251 KB)
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Inhibitory Antibodies User Guide (603 KB)
Références
[1]. Lau D et al. Role of c-Met/β1 integrin complex in the metastatic cascade in breast cancer. JCI Insight. 2021 Jun 22;6(12):e138928. [Content Brief]
[2]. Nigim F, et al. A Monoclonal Antibody Against β1 Integrin Inhibits Proliferation and Increases Survival in an Orthotopic Model of High-Grade Meningioma. Targeted oncology. 2019 Aug;14(4):479-489. [Content Brief]
[3]. Lee TJ, et al. Enhancing Therapeutic Efficacy of Oncolytic Herpes Simplex Virus-1 with Integrin β1 Blocking Antibody OS2966. Molecular cancer therapeutics. 2019 Jun;18(6):1127-1136. [Content Brief]
[4]. Nwagwu CD, et al. Convection-Enhanced Delivery of a First-in-Class Anti-β1 Integrin Antibody for the Treatment of High-Grade Glioma Utilizing Real-Time Imaging. Pharmaceutics. 2020 Dec 30;13(1):40. [Content Brief]
[5]. Nwagwu CD, et al. Endpoint in ovarian cancer xenograft model predicted by nighttime motion metrics. Lab animal. 2020 Aug;49(8):227-232. [Content Brief]
[6]. Carbonell WS, et al. β1 integrin targeting potentiates antiangiogenic therapy and inhibits the growth of bevacizumab-resistant glioblastoma. Cancer research. 2013 May 15;73(10):3145-54. [Content Brief]
[7]. Lapteva M, et al. Fractional laser ablation for the targeted cutaneous delivery of an anti-CD29 monoclonal antibody - OS2966. Scientific reports. 2019 Jan 31;9(1):1030. [Content Brief]
Calculators
Concentration (start) × Volume (start) = Concentration (final) × Volume (final)
OS-2966 Related Classifications
HY-P990643 Related Classifications
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