Anti-Mouse CD20 Antibody (18B12) is a B cell depleting agent that targets mouse CD20. Anti-Mouse CD20 Antibody (18B12) not only inhibits the growth of mesothelioma, lung cancer and thymoma, but also significantly enhances the efficacy of adenoviral tumor antigen vaccines and induces tumor regression by increasing the number of tumor-specific CD8 + T cells. Anti-Mouse CD20 Antibody (18B12) reduces B cell infiltration into the central nervous system of mice with experimental autoimmune encephalomyelitis, and delays motor dysfunction and neuronal death after spinal cord injury by alleviating inflammatory responses and tissue damage. Anti-Mouse CD20 Antibody (18B12) is widely applicable to research in fields related to mesothelioma, lung cancer, thymoma, experimental autoimmune encephalomyelitis and spinal cord injury [1] [2] [3].
In Vivo, Anti-Mouse CD20 Antibody (18B12) (10 mg/kg; i.v.; single dose on day 0) induces a modest, transient slowing of AB12 mesothelioma growth in BALB/c mice, with up to 60% reduction in tumor burden observed depending on treatment timing[1]. Anti-Mouse CD20 Antibody (18B12) (10 mg/kg; i.v.; single dose on day 0) slows growth of established AB12 mesothelioma in BALB/c mice, with up to 70% reduction in tumor burden observed in mice with 7-day established tumors[1]. Anti-Mouse CD20 Antibody (18B12) (10 mg/kg; i.v.; single dose on day 8 post-tumor inoculation) administered in combination with Ad.E7 vaccination induces marked regression of established TC1 lung cancer in C57BL/6 mice, with 67% of tumors completely regressing and cured mice resistant to rechallenge, accompanied by robust systemic and intratumoral tumor antigen-specific CD8+ T-cell responses[1]. Anti-Mouse CD20 Antibody (18B12) (10 mg/kg; i.v.; single dose on day 0) induces sustained B-cell depletion in healthy mice, with >90% depletion of blood and lymph node B cells, 84% depletion of splenic B cells by day 7, and variable depletion of splenic B-cell subpopulations[1]. Anti-Mouse CD20 Antibody (18B12) (5 mg/kg; i.v.; 3 doses on day 19, day 22, day 25 after reaching EAE score ≥2.5) potently depletes 94% of total splenic B cells and reduces CNS-infiltrating B cell infiltrates by up to 77% in wild-type C57BL/6 mice with chronic EAE, but does not improve clinical disease, serum antibody levels, or spinal cord myelination[2]. Anti-Mouse CD20 Antibody (18B12) (30 mg/kg; i.p.; two doses at 1 hour and 6 hours after injury) reduces spinal cord tissue damage, improves hindlimb motor function, inhibits NF-κB pathway activation, lowers proinflammatory mediator and cytokine expression, and reduces immune cell infiltration/activation in a mouse model of SCI[3].
In Vitro, Anti-Mouse CD20 Antibody (18B12) (4.35 μg/μl; 1 h pre-injury pretreatment, 24 h post-injury in medium) reduces cell death and nitric oxide production in postnatal day 6 mouse spinal cord organotypic slices 24 h after mechanical damage[3].
References:
[1]. Kim S, et al. B-cell depletion using an anti-CD20 antibody augments antitumor immune responses and immunotherapy in nonhematopoetic murine tumor models. J Immunother. 2008;31(5):446-457.
[2]. Tacke S, et al. Effects of a Fully Humanized Type II Anti-CD20 Monoclonal Antibody on Peripheral and CNS B Cells in a Transgenic Mouse Model of Multiple Sclerosis. Int J Mol Sci. 2022;23(6):3172. Published 2022 Mar 15.
[3]. Casili G, et al. B-Cell Depletion with CD20 Antibodies as New Approach in the Treatment of Inflammatory and Immunological Events Associated with Spinal Cord Injury. Neurotherapeutics. 2016;13(4):880-894.
In Vivo, Anti-Mouse CD20 Antibody (18B12) (10 mg/kg; i.v.; single dose on day 0) induces a modest, transient slowing of AB12 mesothelioma growth in BALB/c mice, with up to 60% reduction in tumor burden observed depending on treatment timing[1]. Anti-Mouse CD20 Antibody (18B12) (10 mg/kg; i.v.; single dose on day 0) slows growth of established AB12 mesothelioma in BALB/c mice, with up to 70% reduction in tumor burden observed in mice with 7-day established tumors[1]. Anti-Mouse CD20 Antibody (18B12) (10 mg/kg; i.v.; single dose on day 8 post-tumor inoculation) administered in combination with Ad.E7 vaccination induces marked regression of established TC1 lung cancer in C57BL/6 mice, with 67% of tumors completely regressing and cured mice resistant to rechallenge, accompanied by robust systemic and intratumoral tumor antigen-specific CD8+ T-cell responses[1]. Anti-Mouse CD20 Antibody (18B12) (10 mg/kg; i.v.; single dose on day 0) induces sustained B-cell depletion in healthy mice, with >90% depletion of blood and lymph node B cells, 84% depletion of splenic B cells by day 7, and variable depletion of splenic B-cell subpopulations[1]. Anti-Mouse CD20 Antibody (18B12) (5 mg/kg; i.v.; 3 doses on day 19, day 22, day 25 after reaching EAE score ≥2.5) potently depletes 94% of total splenic B cells and reduces CNS-infiltrating B cell infiltrates by up to 77% in wild-type C57BL/6 mice with chronic EAE, but does not improve clinical disease, serum antibody levels, or spinal cord myelination[2]. Anti-Mouse CD20 Antibody (18B12) (30 mg/kg; i.p.; two doses at 1 hour and 6 hours after injury) reduces spinal cord tissue damage, improves hindlimb motor function, inhibits NF-κB pathway activation, lowers proinflammatory mediator and cytokine expression, and reduces immune cell infiltration/activation in a mouse model of SCI[3].
In Vitro, Anti-Mouse CD20 Antibody (18B12) (4.35 μg/μl; 1 h pre-injury pretreatment, 24 h post-injury in medium) reduces cell death and nitric oxide production in postnatal day 6 mouse spinal cord organotypic slices 24 h after mechanical damage[3].
References:
[1]. Kim S, et al. B-cell depletion using an anti-CD20 antibody augments antitumor immune responses and immunotherapy in nonhematopoetic murine tumor models. J Immunother. 2008;31(5):446-457.
[2]. Tacke S, et al. Effects of a Fully Humanized Type II Anti-CD20 Monoclonal Antibody on Peripheral and CNS B Cells in a Transgenic Mouse Model of Multiple Sclerosis. Int J Mol Sci. 2022;23(6):3172. Published 2022 Mar 15.
[3]. Casili G, et al. B-Cell Depletion with CD20 Antibodies as New Approach in the Treatment of Inflammatory and Immunological Events Associated with Spinal Cord Injury. Neurotherapeutics. 2016;13(4):880-894.