InVivoMAb anti-mouse/human osteopontin (SPP1)

Catalog #BE0372
Clone:
100D3
Reactivities:
Mouse, Human

$172.00 - $4,494.00

$172.00 - $4,494.00

Choose an Option...
  • 100 mg - $4,494.00
  • 50 mg - $3,175.00
  • 25 mg - $2,109.00
  • 5 mg - $630.00
  • 1 mg - $172.00
  • Custom Amount (Quotes Only)
In stock
Only %1 left

Product Details

The 100D3 monoclonal antibody reacts with mouse and human osteopontin (OPN), also known as SPP1. Osteopontin is a secreted arginine-glycine-aspartic acid (RGD)-containing glycoprotein that was originally isolated from bone. Osteopontin has been found in kidney, vascular tissues, biological fluids, and various tumor tissues. Osteopontin interacts with integrins and CD44 and regulates diverse biological processes including bone development, immune responses, and oncogenesis. Osteopontin is elevated in human colorectal cancer and is thought to function as an immune checkpoint. The 100D3 antibody is a blocking antibody that has been shown to increase the efficacy of tumor-specific CTLs in killing colon tumor cells in vitro and suppress colon tumor growth in tumor-bearing mice in vivo.

Specifications

Isotype Mouse IgG2c, Īŗ
Recommended Isotype Control(s) InVivoMAb mouse IgG2c isotype control, anti-dengue virus
Recommended Dilution Buffer InVivoPure pH 7.0 Dilution Buffer
Conjugation This product is unconjugated. Conjugation is available via our Antibody Conjugation Services.
Immunogen Recombinant mouse OPN protein
Reported Applications in vivo OPN neutralization
in vitro OPN neutralization
ELISA
Formulation PBS, pH 7.0
Contains no stabilizers or preservatives
Endotoxin <2EU/mg (<0.002EU/μg)
Determined by LAL gel clotting assay
Purity >95%
Determined by SDS-PAGE
Sterility 0.2 µm filtration
Purification Protein A
RRID AB_2927509
Molecular Weight 150 kDa
Storage The antibody solution should be stored at the stock concentration at 4°C. Do not freeze.
in vivo OPN neutralization, in vitro OPN neutralization, ELISA
Klement, J. D., et al. (2021). "Osteopontin Blockade Immunotherapy Increases Cytotoxic T Lymphocyte Lytic Activity and Suppresses Colon Tumor Progression" Cancers (Basel) 13(5). PubMed

Human colorectal cancers are mostly microsatellite-stable with no response to anti-PD-1 blockade immunotherapy, necessitating the development of a new immunotherapy. Osteopontin (OPN) is elevated in human colorectal cancer and may function as an immune checkpoint. We aimed at elucidating the mechanism of action of OPN and determining the efficacy of OPN blockade immunotherapy in suppression of colon cancer. We report here that OPN is primarily expressed in tumor cells, myeloid cells, and innate lymphoid cells in human colorectal carcinoma. Spp1 knock out mice exhibit a high incidence and fast growth rate of carcinogen-induced tumors. Knocking out Spp1 in colon tumor cells increased tumor-specific CTL cytotoxicity in vitro and resulted in decreased tumor growth in vivo. The OPN protein level is elevated in the peripheral blood of tumor-bearing mice. We developed four OPN neutralization monoclonal antibodies based on their efficacy in blocking OPN inhibition of T cell activation. OPN clones 100D3 and 103D6 increased the efficacy of tumor-specific CTLs in killing colon tumor cells in vitro and suppressed colon tumor growth in tumor-bearing mice in vivo. Our data indicate that OPN blockade immunotherapy with 100D3 and 103D6 has great potential to be further developed for colorectal cancer immunotherapy and for rendering a colorectal cancer response to anti-PD-1 immunotherapy.

in vivo OPN neutralization, in vitro OPN neutralization, ELISA
Klement, J. D., et al. (2021). "Osteopontin Blockade Immunotherapy Increases Cytotoxic T Lymphocyte Lytic Activity and Suppresses Colon Tumor Progression" Cancers (Basel) 13(5). PubMed

Human colorectal cancers are mostly microsatellite-stable with no response to anti-PD-1 blockade immunotherapy, necessitating the development of a new immunotherapy. Osteopontin (OPN) is elevated in human colorectal cancer and may function as an immune checkpoint. We aimed at elucidating the mechanism of action of OPN and determining the efficacy of OPN blockade immunotherapy in suppression of colon cancer. We report here that OPN is primarily expressed in tumor cells, myeloid cells, and innate lymphoid cells in human colorectal carcinoma. Spp1 knock out mice exhibit a high incidence and fast growth rate of carcinogen-induced tumors. Knocking out Spp1 in colon tumor cells increased tumor-specific CTL cytotoxicity in vitro and resulted in decreased tumor growth in vivo. The OPN protein level is elevated in the peripheral blood of tumor-bearing mice. We developed four OPN neutralization monoclonal antibodies based on their efficacy in blocking OPN inhibition of T cell activation. OPN clones 100D3 and 103D6 increased the efficacy of tumor-specific CTLs in killing colon tumor cells in vitro and suppressed colon tumor growth in tumor-bearing mice in vivo. Our data indicate that OPN blockade immunotherapy with 100D3 and 103D6 has great potential to be further developed for colorectal cancer immunotherapy and for rendering a colorectal cancer response to anti-PD-1 immunotherapy.

    • Immunology and Microbiology
    • ,
    • Stem Cells and Developmental Biology
    Dermal TRPV1 innervations engage a macrophage- and fibroblast-containing pathway to activate hair growth in mice.

    In Developmental Cell on 4 November 2024 by Ben-Shaanan, T. L., Knƶpper, K., et al.

    Pain, detected by nociceptors, is an integral part of injury, yet whether and how it can impact tissue physiology and recovery remain understudied. Here, we applied chemogenetics in mice to locally activate dermal TRPV1 innervations in naive skin and found that it triggered new regenerative cycling by dormant hair follicles (HFs). This was preceded by rapid apoptosis of dermal macrophages, mediated by the neuropeptide calcitonin gene-related peptide (CGRP). TRPV1 activation also triggered a macrophage-dependent induction of osteopontin (Spp1)-expressing dermal fibroblasts. The neuropeptide CGRP and the extracellular matrix protein Spp1 were required for the nociceptor-triggered hair growth. Finally, we showed that epidermal abrasion injury induced Spp1-expressing dermal fibroblasts and hair growth via a TRPV1 neuron and CGRP-dependent mechanism. Collectively, these data demonstrated a role for TRPV1 nociceptors in orchestrating a macrophage and fibroblast-supported mechanism to promote hair growth and enabling the efficient restoration of this mechano- and thermo-protective barrier after wounding. Copyright Ā© 2024 The Authors. Published by Elsevier Inc. All rights reserved.