OS-2966 - KKL Med Inc.

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OS-2966

目录号 : KM32887

Data Sheet 产品使用指南

OS-2966 是一种人源化的抗 CD29 (β1 整合素/ITGB1) 中和性单克隆抗体 (huIgG1κ)。OS-2966 阻断整合素 β1 信号传导，抑制肿瘤细胞增殖、侵袭、迁移和间充质表型，并增强溶瘤单纯疱疹病毒-1（oHSV）和抗血管生成治疗的疗效。OS-2966 可用于三阴性乳腺癌、高级别脑膜瘤、胶质母细胞瘤以及卵巢癌的相关研究。

规格	价格	是否有货	数量
1mg	询价	In-stock

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生物活性

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.

IC₅₀&Target

CD29

体外研究

Anti-cancer

OS-2966 (20 μg/mL; 0-24 h) 可在 MDA-MB-231 人三阴性乳腺癌腺癌细胞中破坏 c-Met/β1 整合蛋白复合物，使用条件为 20 μg/mL、作用时长最长 24 小时。
OS-2966 (20 μg/mL; 24 h) 可逆转 AP21967 诱导的 MDA-MB-231-iDimerize-c-Met-β1 人三阴性乳腺腺癌细胞中 Snail 和 FOXC2 间质转录因子的上调，可逆转 AP21967 诱导的 MDA-MB-231-iDimerize-c-Met-β1 人三阴性乳腺腺癌细胞的间充质形态变化。
OS-2966 (20 μg/mL; 24 h) 可降低 MDA-MB-231-BO 骨趋向性人三阴性乳腺腺癌细胞中多种间质转录因子 (Snail、FOXC1、FOXC2、Slug、ZEB1、ZEB2) 的表达。
OS-2966 (0.2-100.0 μg/mL; 3 days) 可抑制接种于层粘连蛋白包被塑料上的 NF2 野生型 IOMM-Lee 间变性脑膜瘤细胞的活力，阻断其贴附并诱导细胞变圆。
OS-2966 (50 μg/mL; 3 hours) 可抑制铺层粘连蛋白的塑料培养板上生长的 NF2-野生型间变性脑膜瘤细胞 IOMM-Lee 中 AKT (Ser473) 和 ERK1/2 的磷酸化 (但不抑制 FAK (Tyr397) 的磷酸化)，而在未包被的塑料培养板上生长的细胞中未观察到该信号通路的变化。

Innate Immunity

OS-2966 (感染 oHSV 后 4 小时) 可抑制巨噬细胞向 oHSV 感染及未感染的 LN229 胶质母细胞瘤细胞迁移。

Anti-cancer Viral Infection

OS-2966 (10 μg/mL; post oHSV treatment, during co-culture with macrophages) 可增强与 RAW264.7 巨噬细胞共培养的 GBM30 原代 GBM 细胞中 oHSV 的复制。

Others

OS-2966 (1-5 mg/mL; 12 h) 可实现针对猪全层耳皮肤的点阵激光消融靶向经皮递送，在有效激光条件下的最大皮肤沉积量为 3.665 μg/cm²，局部皮肤保留率≥70%，同时将透皮渗透降至最低。

Real Time qPCR

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)

Concentration:

20 μg/mL

Incubation Time:

24 hours

Result:

Reversed the AP21967-induced upregulation of Snail and FOXC2.

Real Time qPCR

Cell Line:

MDA-MB-231-BO bone-seeking human triple-negative breast adenocarcinoma cells

Concentration:

20 μg/mL

Incubation Time:

24 hours

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.

Cell Invasion Assay

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)

Concentration:

20 μg/mL

Incubation Time:

24 hours

Result:

Reversed the AP21967-induced increase in invasiveness.

Cell Viability Assay

Cell Line:

NF2-deficient MN3 patient-derived anaplastic meningioma sphere cells

Concentration:

6.8, 12.5, 25.0, 50.0, 100.0 μg/mL

Incubation Time:

5 days

Result:

Suppressed cell viability by approximately 50% relative to untreated controls.
Showed no apparent dose-response effect across the tested concentrations.

Cell Viability Assay

Cell Line:

NF2-wild-type IOMM-Lee anaplastic meningioma cells (on uncoated plastic)

Concentration:

0.2, 0.8, 4.0, 20.0, 100.0 μg/mL

Incubation Time:

4 days

Result:

Had no effect on cell viability at any tested concentration.
Maintained relative viability near 100% across all doses.

Cell Viability Assay

Cell Line:

NF2-wild-type IOMM-Lee anaplastic meningioma cells (on laminin-coated plastic)

Concentration:

0.2, 0.8, 4.0, 20.0, 100.0 μg/mL (viability assay); 50 μg/mL (morphology assessment)

Incubation Time:

3 days (viability assay); 3 hours (morphology assessment)

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.

Western Blot Analysis

Cell Line:

NF2-deficient MN3 patient-derived anaplastic meningioma sphere cells

Concentration:

50 μg/mL

Incubation Time:

3 hours

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.

Western Blot Analysis

Cell Line:

NF2-wild-type IOMM-Lee anaplastic meningioma cells (on uncoated or laminin-coated plastic)

Concentration:

50 μg/mL

Incubation Time:

3 hours

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.

Cell Viability Assay

Cell Line:

NF2-deficient MN8 patient-derived anaplastic meningioma cells

Concentration:

12.5, 25.0, 50.0 μg/mL (viability assay); 50 μg/mL (attachment assay)

Incubation Time:

4 days (viability assay); 48 hours (attachment assay)

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.

体内研究

Anti-cancer Cell Cycle Regulation

OS-2966 (20 mg/kg；腹腔注射；每周 2 次；持续 6 周) 可显著延长原位植入患者来源高级别脑膜瘤的小鼠的总生存期，并降低肿瘤细胞增殖水平。

Anti-cancer Viral Infection

OS-2966 (5 mg/kg；腹腔注射；每周 2 次) 可增强皮下胶质母细胞瘤异种移植物中 oHSV 的复制及抗肿瘤效力，使病毒总通量显著增加并抑制肿瘤生长。
OS-2966 (5 mg/kg；腹腔注射；oHSV 给药前 1 天，之后每周 2 次) 可增强原位三阴性乳腺癌异种移植物中 oHSV 的复制能力与抗肿瘤效力，至第 21 天时肿瘤体积缩小 10.9 倍，应答率达 100%，且 50%的肿瘤完全消退。

Anti-cancer

OS-2966 (5 mg/kg；瘤内注射；于溶瘤疱疹病毒给药前 2 天开始，随后每周 2 次；持续 1 个月) 可增强溶瘤疱疹病毒在颅内胶质母细胞瘤异种移植模型中的抗肿瘤效力，进而缩小肿瘤体积并提高小鼠存活率。
OS-2966 (10 mg/kg；腹腔注射；每周 2 次，采用 3/4 天交替给药间隔) 单药治疗可显著降低腹腔内接种 ES-2 卵巢癌异种移植物的雌性无胸腺裸鼠 Foxn1^nu 的腹水体积。
OS-2966 (1 mg/kg；腹腔注射；每周 2 次；与 1 mg/kg Bevacizumab 交替给药) 在抑制未接受过 Bevacizumab 治疗的皮下胶质母细胞瘤生长方面，疗效与标准剂量贝伐珠单抗相当。

Others

OS-2966 (5-30 mg/kg; 静脉注射) 以最高 30 mg/kg 的剂量经全身静脉给予非人灵长类动物后耐受性良好，仅在剂量高于 5 mg/kg 时出现轻微、可逆的血液学及血清生化指标变化。

Anti-cancer Apoptosis

OS-2966 (1-5 mg/kg；腹腔注射；每周 2 次) 可显著抑制皮下 Bevacizumab 耐药性胶质母细胞瘤的生长，其中 5 mg/kg 剂量可使 56%的受试小鼠实现肿瘤完全消退。
OS-2966 (总剂量 160 μg；瘤内给药；持续递送；28 天) 可诱导对 Bevacizumab 耐药的原位胶质母细胞瘤完全消退，抑制肿瘤侵袭，并引发大量肿瘤细胞凋亡。

Animal Model:	SCID (7-8-week-old female; orthotopic subdural implantation of patient-derived MN3 anaplastic meningioma cells)
Dosage:	20 mg/kg (survival study); 20 mg/kg (mechanism-of-action studies)
Administration:	i.p.; twice weekly; 6 weeks (survival study); i.p.; two doses over 1 week (mechanism-of-action studies)
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.

Animal Model:

Athymic nu/nu (female, 4 weeks old, outbred)

Dosage:

5 mg/kg

Administration:

i.p.; twice a week

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.

Animal Model:

Athymic nu/nu (female, 4 weeks old, outbred)

Dosage:

5 mg/kg

Administration:

i.p.; 1 day prior to oHSV, then twice a week

Result:

Increased viral replication to a total flux of 311398.3 compared to 89636.5 for oHSV + control IgG.
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.

Animal Model:

Athymic nu/nu (female, 4 weeks old, outbred)

Dosage:

5 mg/kg

Administration:

intratumoral; starting 2 days prior to oHSV, then twice a week; 1 month

Result:

Significantly reduced tumor size compared to oHSV + control IgG.
Significantly improved mouse survival compared to either monotherapy.

Animal Model:

athymic mice (5- to 8-week-old female; subcutaneous xenograft of Bevacizumab-resistant BRG3 human glioblastoma cells)

Dosage:

1 mg/kg; 5 mg/kg

Administration:

i.p.; twice weekly

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.

Animal Model:

athymic mice (5- to 8-week-old female; orthotopic xenograft of Bevacizumab-resistant BRG3 human glioblastoma cells)

Dosage:

160 μg total

Administration:

intratumoral; continuous delivery; 28 days

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.

分子量

145.5 kDa

运输条件

Shipping with dry ice.

种属反应性

Human

同种型

Human IgG1 kappa

Accession号

P05556

应用

ELISA, FACS, Functional assay

基因 ID

3688 [NCBI]

推荐同型对照抗体

Human IgG1 kappa, Isotype Control

Data Sheet

产品使用指南

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.

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.

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.

The molarity calculator equation

Mass (g) = Concentration (mol/L) × Volume (L) × Molecular Weight (g/mol)

质量

浓度

体积

分子量*

重置计算

The dilution calculator equation

Concentration (start) × Volume (start) = Concentration (final) × Volume (final)
This equation is commonly abbreviated as: C1V1 = C2V2

浓度

体积

浓度

体积

重置计算

动物实验计算换算器

第一步：请输入基本实验信息（考虑到实验过程中的损耗，建议多配一只动物的药量）

给药剂量

mg/kg

动物平均体重

每只动物给药体积

动物数量

只

第二步：请输入动物体内配方组成（配方适用于不溶于水的药物；不同批次药物配方比例不同，请联系客服为您提供正确的澄清溶液配方）

% DMSO

% Tween 80

% ddH₂O

% DMSO

计算重置

计算结果:

工作液浓度： mg/ml；

DMSO母液配制方法： mg 药物溶于 μL DMSO溶液（母液浓度 mg/mL，注：如该浓度超过该批次药物DMSO溶解度，请先联系客服）；

体内配方配制方法：取 μL DMSO母液，加入 μL PEG300，混匀澄清后加入μL Tween 80，混匀澄清后加入 μL ddH₂O，混匀澄清。

配置后的溶液总体积：

注意：1. 首先保证母液是澄清的；
2. 一定要按照顺序依次将溶剂加入，进行下一步操作之前必须保证上一步操作得到的是澄清的溶液，可采用涡旋、超声或水浴加热等物理方法助溶。

Other Forms of Rapamycin:

KKL 顾客使用本产品发表的 0 篇科研文献

The molarity calculator equation

The dilution calculator equation

动物实验计算换算器