Anti-CD146 Antibody (AA98)

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Anti-CD146 Antibody (AA98) is an antibody targeting CD146 and an angiogenesis inhibitor. Anti-CD146 Antibody (AA98) blocks the dimerization of CD146 as well as its downstream PI3K/AKT, p38 MAPK and NF-κB signaling pathways; it inhibits the expression of MMP9 and ICAM1, epithelial-mesenchymal transition (EMT), and the proliferation, migration and tube formation of endothelial cells. Anti-CD146 Antibody (AA98) enhances radiation-induced cancer cell apoptosis and survival inhibition, reduces tumor microvessel density, and suppresses tumor growth, invasion and vasculogenic mimicry. Anti-CD146 Antibody (AA98) can be used in research related to cervical cancer, liver cancer, malignant phyllodes tumor of the breast, uveal melanoma, leiomyosarcoma, pancreatic cancer, other tumors and angiogenesis.

For research use only. We do not sell to patients.

Anti-CD146 Antibody (AA98) Chemical Structure

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PI3Kα PI3Kβ PI3Kγ PI3Kδ PI3KC2α PI3KC2β PI3KC2γ Vps34 PI3K PI3KC3 p120γ

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Akt Akt1 Akt2 Akt3

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p38 MAPK Akt1 p38α p38β MAPK13 p38δ p38γ

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NF-κB NF-κB1/p50 RelA/p65 RelB c-Rel

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MMP-1 MMP-2 MMP-3 MMP-8 MMP-9 MMP-13 MMP-14 MMP-17 ADAM10 ADAM17 MMP-7 MMP-12 MMP-10 MMP ADAM8 MMP-19

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Caspase 1 Caspase 2 Caspase 3 Caspase 4 Caspase 5 Caspase 6 Caspase 7 Caspase 8 Caspase 9 Caspase 10 Caspase 12 Caspase Caspase 11 Caspase-13

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Bcl-2 Bcl-xL Bcl-W Mcl-1 Bfl-1 Bcl-B Bax Bak Bim BNIP3 Bad

Biological Activity
Purity & Documentation
References
Customer Review

Description

Isotype

Mouse IgG2a kappa

Recommend Isotype Controls

Mouse IgG2a kappa, Isotype Control

Species Reactivity

Human

IC₅₀ & Target^[1]^[2]

CD146

MMP-9

Caspase 3

In Vitro

Anti-CD146 Antibody (AA98) (10 μg/mL; 30 min radiation, 2-week post-irradiation incubation) significantly reduces the survival fraction of irradiated SiHa human cervical squamous cell carcinoma cells and enhances their radiosensitivity^[1].
Anti-CD146 Antibody (AA98) (10 μg/mL; 30 min radiation, 72 h, 7 days post-irradiation) significantly enhances radiation-induced apoptosis in SiHa human cervical squamous cell carcinoma cells at 72 h and 7 days post-irradiation, upregulates the expression of Caspase 3, and downregulates the expression of Bcl-XL protein^[1].
Anti-CD146 Antibody (AA98) (10-50 μg/mL; 30-90 min) inhibits the nuclear translocation of NF-κB p65 and p50, suppresses NF-κB activation, and reduces the phosphorylation of p38 MAPK in primary human umbilical vein endothelial cells induced by SMMC 7721-CM^[2].
Anti-CD146 Antibody (AA98) (50 μg/mL; 24 h) inhibits the SMMC 7721-CM-enhanced MMP-9 activity and mRNA expression, suppresses ICAM-1 mRNA and protein expression, and inhibits cell migration in primary human umbilical vein endothelial cells^[2].
Anti-CD146 Antibody (AA98) (50 μg/mL; 1 h) specifically binds to CD146 expressed on the surface of human umbilical vein endothelial cells (HUVEC), as observed by immunofluorescence staining^[3].
Anti-CD146 antibody (AA98) (150 μg/mL; 16-96 h) inhibits the proliferation, colony formation, migration, invasion and collagen contraction of SYSH-MPT-02 malignant phyllodes tumor cells, and suppresses the activation of the PI3K-AKT signaling pathway by reducing the level of phosphorylated AKT^[4].
Anti-CD146 antibody (AA98) (150 μg/mL; 35 days) inhibits the growth of primary malignant phyllodes tumor organoids^[4].
The anti-CD146 antibody (AA98) directly blocks the interaction between CD146 and DCBLD2 proteins^[4].
Anti-CD146 Antibody (AA98) (100 μg/mL; 6 h) inhibits M17-CM-induced tube formation in primary human retinal microvascular endothelial cells, reducing the total relative tube length by 33.7% after M17-CM treatment and by 36.4% after SP6.5-CM treatment^[5].
Anti-CD146 Antibody (AA98) (50 μg/mL; 24 h) inhibits M17-CM-induced migration of primary human retinal microvascular endothelial cells, reducing the number of migrated cells by approximately 62.6% after M17-CM treatment and by approximately 68.0% after SP6.5-CM treatment^[5].
Anti-CD146 Antibody (AA98) (50 μg/mL; 24 h) inhibits VEGF-induced activation of VEGFR-2, AKT and p38 signaling pathways, as well as nuclear translocation of NF-κB p65, in primary human retinal microvascular endothelial cells^[5].
Anti-CD146 Antibody (AA98) (50 μg/mL; 20 h) inhibits vasculogenic mimicry in M17 and SP6.5 uveal melanoma cells, reducing the total relative tube length by 30.2% in M17 cells and 42.6% in SP6.5 cells^[5].
Anti-CD146 Antibody (AA98) (50 μg/mL) inhibits the activation of the FAK/VE-cadherin signaling pathway in M17 and SP6.5 uveal melanoma cells^[5].
Anti-CD146 Antibody (AA98) (50 μg/mL) inhibits the epithelial-mesenchymal transition process in M17 and SP6.5 uveal melanoma cells, upregulates the expression of E-cadherin, and downregulates the expressions of N-cadherin, vimentin, and snail transcription factor^[5].
Anti-CD146 Antibody (AA98) (40 μg/mL; 24 h) inhibits the migration and invasion of M17 and SP6.5 uveal melanoma cells^[5].
Anti-CD146 Antibody (AA98) (1-100 μg/mL; 48 h) inhibits the proliferation of HUVECs in a dose-dependent manner, with a maximum inhibition rate of up to 62.4% at the concentration of 100 μg/mL, but exerts no inhibitory effect on the proliferation of human melanoma A375 cells^[6].
Anti-CD146 Antibody (AA98) (10 μg/mL; 4 h) reduces the migration capacity of HUVECs towards VEGF/bFGF by 75%^[6].

MedChemExpress (MCE) has not independently confirmed the accuracy of these methods. They are for reference only.

Apoptosis Analysis^[1]

Cell Line:	human cervical squamous cell carcinoma SiHa cells
Concentration:	10 μg/mL (pre-treatment prior to radiation)
Incubation Time:	30 min (radiation); 72 h, 7 days post-irradiation
Result:	Increased the percentage of apoptotic cells in irradiated SiHa cells compared to untreated control cells.

Western Blot Analysis^[1]

Cell Line:	human cervical squamous cell carcinoma SiHa cells
Concentration:	10 μg/mL (pre-treatment prior to radiation)
Incubation Time:	30 min (radiation)
Result:	Up-regulated pro-apoptotic Caspase 3 protein expression in irradiated SiHa cells compared to untreated control cells. Down-regulated anti-apoptotic Bcl-XL protein expression in irradiated SiHa cells compared to untreated control cells.

Immunofluorescence^[3]

Cell Line:	human umbilical vein endothelial cells (HUVEC)
Concentration:	50 μg/mL
Incubation Time:	1 h (each antibody step)
Result:	Intensively bound to CD146-positive HUVEC, resulting in strong fluorescent staining of the cell surface, similar to the engineered AA98 V_H/L fragment.

Cell Proliferation Assay^[4]

Cell Line:	SYSH-MPT-02 malignant breast phyllodes tumor cells
Concentration:	150 μg/mL
Incubation Time:	96 h
Result:	Significantly suppressed cell proliferation, as measured by reduced absorbance at 492 nm in the MTS assay compared to control groups. Inhibited colony formation, migration, invasion, and collagen contraction of cells. Downregulated the level of phosphorylated AKT (p-AKT), while total AKT levels remained unchanged.

Cell Migration Assay ^[5]

Cell Line:	primary human retinal microvascular endothelial cells (HRMEC)
Concentration:	50 μg/mL
Incubation Time:	24 h
Result:	Reduced migrated cell counts from 213.7 cells/vision field (IgG control) to 80.0 cells/vision field with M17-CM. Reduced migrated cell counts from 166.7 cells/vision field (IgG control) to 53.3 cells/vision field with SP6.5-CM.

Western Blot Analysis^[5]

Cell Line:	primary human retinal microvascular endothelial cells (HRMEC)
Concentration:	50 μg/mL
Incubation Time:	24 h
Result:	Significantly reduced VEGF-induced phosphorylation of VEGFR-2 compared to IgG control. Significantly reduced VEGF-induced phosphorylation of AKT compared to IgG control. Significantly reduced VEGF-induced phosphorylation of p38 compared to IgG control.

Cell Invasion Assay^[5]

Cell Line:	uveal melanoma cell lines M17 and SP6.5
Concentration:	40 μg/mL
Incubation Time:	24 h
Result:	Significantly reduced invaded cell counts in M17 compared to IgG control. Significantly reduced invaded cell counts in SP6.5 compared to IgG control.

Cell Proliferation Assay^[6]

Cell Line:	human umbilical vein endothelial cells (HUVECs), human melanoma A375 cells
Concentration:	1 μg/mL, 10 μg/mL, 100 μg/mL
Incubation Time:	48 h
Result:	Inhibited [³H]-thymidine incorporation into HUVEC DNA in a dose-dependent manner: 28.5% inhibition at 1 μg/mL, 43.2% inhibition at 10 μg/mL, and 62.4% inhibition at 100 μg/mL. Showed only 5%-7% inhibition of HUVEC proliferation with isotype-matched control antibody. Exhibited no significant inhibitory effect on A375 melanoma cell proliferation across tested concentrations.

In Vivo

Anti-CD146 Antibody (AA98) (1-15 μg; topical; single dose) inhibits angiogenesis in the chicken CAM model^[3].
Anti-CD146 Antibody (AA98) (0.25 mg/mice; i.p.; twice a week; 24 days) significantly suppresses the growth of malignant breast phyllodes tumor patient-derived xenografts in NOD/SCID mice, associated with reduced PI3K/AKT pathway activation, tumor cell proliferation, and angiogenesis^[4].
Anti-CD146 Antibody (AA98) (4 μg; subretinal; single administration) reduces uveal melanoma tumor growth by 71.2%, inhibits angiogenesis by 54.7%, and suppresses vasculogenic mimicry by 40.6% in BALB/C nude mice bearing subretinal M17 cell xenografts^[5].
Anti-CD146 Antibody (AA98) (4 μg; subretinal; single administration) reduces uveal melanoma tumor growth by 78.4%, inhibits angiogenesis by 55.0%, and suppresses vasculogenic mimicry by 64.9% in BALB/C nude mice bearing subretinal SP6.5 cell xenografts^[5].
Anti-CD146 Antibody (AA98) (10 mg/kg; i.p.; twice per week; 28 days) inhibits human hepatocellular carcinoma xenograft growth in BALB/c nude mice by 72% and prevents metastasis^[6].
Anti-CD146 Antibody (AA98) (10 mg/kg; i.p.; twice per week; 24 days) inhibits human leiomyosarcoma xenograft growth in BALB/c nude mice by 50%, prevents metastasis, and alters tumor blood vessel structure^[6].
Anti-CD146 Antibody (AA98) (10 mg/kg; i.p.; twice per week; 18 days) inhibits human pancreatic cancer xenograft growth in BALB/c nude mice by 41% and reduces tumor microvessel density by approximately 70%^[6].
¹³¹I-labeled Anti-CD146 Antibody (AA98) (97 μg; i.p.; single dose; 18 days) inhibits human pancreatic cancer xenograft growth in BALB/c nude mice by 75% and reduces tumor microvessel density^[6].

MedChemExpress (MCE) has not independently confirmed the accuracy of these methods. They are for reference only.

Animal Model:	white Leghorn (6-day-old embryos from fertilized eggs)^[3]
Dosage:	1 μg, 5 μg, 15 μg
Administration:	topical; single dose
Result:	Induced avascular zones around the antibody-applied areas, where blood vessels became slim and pale.

Animal Model:	NOD/SCID (6-week-old female)^[4]
Dosage:	0.25 mg/mice
Administration:	i.p.; twice a week; 24 days
Result:	Inhibited growth of malignant phyllodes tumor patient-derived xenografts, with significantly smaller tumor volumes compared to control groups over the 24-day treatment period. Decreased levels of phospho-AKT in treated tumor tissues. Reduced Ki67 staining index in treated tumor tissues. Lowered density of CD31+ vascular endothelium in treated tumor tissues.

Animal Model:	BALB/C nude (4-6 weeks old)^[5]
Dosage:	4 μg
Administration:	subretinal; single administration
Result:	Reduced tumor size by 71.2% compared to the IgG control group. Reduced microvessel density by 54.7% relative to the IgG control group. Suppressed vasculogenic mimicry formation by 40.6% relative to the IgG control group.\nReduced tumor size by 78.4% compared to the IgG control group. Reduced microvessel density by 55.0% relative to the IgG control group. Suppressed vasculogenic mimicry formation by 64.9% relative to the IgG control group.

Animal Model:	BALB/c nude mice (female, 6-week-old, ~20 g, subcutaneous xenograft model with SSMC 7721 cells)^[6]
Dosage:	10 mg/kg
Administration:	i.p.; twice per week; 28 days
Result:	Reduced tumor volume significantly compared with PBS controls, with 72% inhibition of tumor growth after 28 days of treatment. Prevented metastasis, with no metastases detected via histopathologic analysis, whereas 60%-80% of control mice developed lung and lymph node metastases. Caused no toxic effects, and no deaths occurred in the treated group, whereas 20% of control mice died between days 14-16.

Animal Model:	BALB/c nude mice (female, 6-week-old, ~20 g, subcutaneous xenograft model with SK-LMS-1 cells)^[6]
Dosage:	10 mg/kg
Administration:	i.p.; twice per week; 24 days
Result:	Reduced tumor volume significantly compared with mIgG and PBS controls, with 50% inhibition of tumor growth after 24 days of treatment. Prevented metastasis, with no metastases detected via histopathologic analysis, whereas 60%-80% of control mice developed lung and lymph node metastases. Caused no toxic effects, and no deaths occurred in the treated group, whereas 20% of control mice died between days 14-16. Induced blood vessels with narrowed lumina surrounded by extracellular matrix material, some occluded by thrombi, via histologic analysis of treated tumors.

Animal Model:	BALB/c nude mice (female, 6-week-old, ~20 g, subcutaneous xenograft model with SW1990 cells)^[6]
Dosage:	10 mg/kg
Administration:	i.p.; twice per week; 18 days
Result:	Reduced tumor volume significantly compared with mIgG and PBS controls, with 41% inhibition of tumor growth after 18 days of treatment. Reduced microvessel density in treated tumors by approximately 70% compared with mIgG-treated tumors. Prevented metastasis, with no metastases detected via histopathologic analysis, whereas 60%-80% of control mice developed lung and lymph node metastases. Caused no toxic effects, and no deaths occurred in the treated group, whereas 20% of control mice died between days 14-16.

Animal Model:	BALB/c nude mice (female, 6-week-old, ~20 g, subcutaneous xenograft model with SW1990 cells)^[6]
Dosage:	97 μg (with 18.5 MBq [¹³¹I] activity)
Administration:	i.p.; single dose; 18 days
Result:	Reduced tumor volume significantly compared with [¹³¹I]-mIgG controls, with 75% inhibition of tumor growth after 18 days of treatment. Reduced microvessel density in treated tumors compared with [¹³¹I]-mIgG-treated tumors.

Gene ID

4162 [NCBI]

Accession

P43121

Target

MUC18/MCAM/CD146

Application

ELISA, FACS, Functional assay

Conjugated

Unconjugated

Reconsititution

The product can be reconstituted/diluted with sterile PBS or saline.

Formulation

Please refer to the lot-specific COA for specific buffer information.

Storage

Please store the product under the recommended conditions in the Certificate of Analysis.

Purity & Documentation

Inhibitory Antibodies User Guide (603 KB)

References

[1]. Cheng H, et al. Inhibiting CD146 by its Monoclonal Antibody AA98 Improves Radiosensitivity of Cervical Cancer Cells. Med Sci Monit. 2016;22:3328-3333. Published 2016 Sep 20.

[2]. Bu P, et al. Anti-CD146 monoclonal antibody AA98 inhibits angiogenesis via suppression of nuclear factor-kappaB activation. Mol Cancer Ther. 2006;5(11):2872-2878.

[3]. Lin Y, et al. A novel antibody AA98 V(H)/L directed against CD146 efficiently inhibits angiogenesis. Anticancer Res. 2007;27(6B):4219-4224.

[4]. Chen J, et al. CD146 promotes malignant progression of breast phyllodes tumor through suppressing DCBLD2 degradation and activating the AKT pathway. Cancer Commun (Lond). 2023;43(11):1244-1266.

[5]. Zhang R, et al. Inhibition of CD146 lessens uveal melanoma progression through reducing angiogenesis and vasculogenic mimicry. Cell Oncol (Dordr). 2022;45(4):557-572.

[6]. Yan X, et al. A novel anti-CD146 monoclonal antibody, AA98, inhibits angiogenesis and tumor growth. Blood. 2003;102(1):184-191.