huATN-658 

huATN-658 is an inhibitor that specifically targets the DIII domain of human urokinase plasminogen activator receptor (uPAR). huATN-658 neutralizes uPAR function by blocking the interaction between uPAR and integrins, without interfering with the binding of uPA or vitronectin to uPAR. huATN-658 inhibits the proliferation and invasion of breast cancer cells, slows the growth of primary breast tumors, reduces breast cancer-induced bone lesions and decreases osteoclast activity. huATN-658 also alters the gene expression of the TGF-β receptor complex signaling pathway. huATN-658 exerts synergistic anticancer effects when combined with Zoledronic Acid (HY-13777), and does not cause physiological or behavioral abnormalities in immunodeficient mice. huATN-658 can be used in research related to breast cancer, metastatic breast cancer and breast cancer-induced bone disease^[1][2].

Human IgG1 kappa

Human IgG1 kappa, Isotype Control

Human

PLAUR/uPAR/CD87

huATN-658 (50 μg/mL; 48 h) significantly inhibits the proliferation of human breast cancer cell lines MDA-MB-231 and Hs578T in vitro, but exerts no such effect on MDA-BoM-1833 cells^[1].
huATN-658 (50 μg/mL; 18 h) significantly inhibits the invasion of human breast cancer cell lines MDA-MB-231, Hs578T and MDA-BoM-1833 in vitro^[1].
huATN-658 (50 μg/mL) alters the transcriptome of human breast cancer MDA-MB-231 cells in vitro, and differentially regulates 61 genes, among which the most highly enriched pathway is the TGF-β receptor complex signaling pathway^[1].
huATN-658 effectively inhibits invasion, migration and proliferation of human prostate cancer cells in vitro^[2].

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

huATN-658 (10 mg·kg^-1; intraperitoneal; twice a week; 5 weeks) significantly reduces primary mammary tumor volume in female CD-1 nude mice bearing orthotopic MDA-MB-231 xenografts^[1].
huATN-658 (10 mg·kg^-1; intraperitoneal; twice a week; 10 weeks) significantly reduces skeletal lesion progression, osteoclast number, and tumor cell proliferation in female CD-1 nude mice with intratibial MDA-MB-231 xenografts^[1].
huATN-658 (10 mg·kg^-1; intraperitoneal; twice a week; 6 weeks) reduces skeletal lesion development in female CD-1 nude mice with intratibial MDA-BoM-1833 xenografts^[1].
huATN-658 causes a significant reduction in primary breast tumor growth in immunocompromised mice bearing MDA-MB-231 breast cancer xenografts^[2].
huATN-658 significantly reduces breast cancer-induced skeletal lesions and intratumoral bone microenvironment growth in immunocompromised mice, with enhanced efficacy when combined with zoledronic acid^[2].

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

22943  [NCBI]

O94907

ELISA, FACS, Functional assay

Unconjugated

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

146.34 kDa

Liquid

Colorless to light yellow

[huATN658]

Shipping with dry ice.

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

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

• 
  Flow Cytometry analysis of Hela cells with huATN-658 (HY-P990552A, red). Cells were fixed with 4% paraformaldehyde and permeabilised with 90% methanol. Then cells were stained with the primary antibody at 1/200 dilution for an hour at 4℃. Goat Anti-Human IgG H&L (AF488) (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 huuPAR-Fc can bind huATN-658. The EC₅₀ for this effect is 51.98 ng/mL.

• [1]. Mahmood N, et al. uPAR antibody (huATN-658) and Zometa reduce breast cancer growth and skeletal lesions. Bone Res. 2020;8:18. Published 2020 Apr 17.  [Content Brief]

  [2]. Mahmood N, et al. Fibrinolytic System and Cancer: Diagnostic and Therapeutic Applications. Int J Mol Sci. 2021;22(9):4358. Published 2021 Apr 22.  [Content Brief]