Anti-Mouse CSF1R/CD115 Antibody (AFS98) 

Anti-Mouse (CSF1R/CD115) Antibody (AFS98) is an anti-mouse CSF1R IgG2a antibody inhibitor derived from rats. Anti-Mouse (CSF1R/CD115) Antibody (AFS98) inhibits M-CSF-dependent colony formation and cell growth by blocking the binding of M-CSF to its receptor. Anti-Mouse (CSF1R/CD115) Antibody (AFS98) can be used for the researches of inflammation, metabolic disease, cardiovascular disease and neurological disease, such as such as stroke, diabetes and arthritis^[1][2][3][4].

Rat IgG2a kappa

Rat IgG2a kappa, Isotype Control

Mouse

CSF1R/CD115

The antibody framework is stable, specific and adaptable, and has the ability to bind both antigens and endogenous immune receptors. Monoclonal antibodies have several derivatives, including bispecific antibodies, antibody-drug conjugates, and antibody fragments, and have significant effects in fields such as immunology and oncology. When designing inhibitory antibodies, considerations include identification of antigen-specific variable regions, choice of expression system, use of multispecific formats, and antibody derivatives based on fragmentation, oligomerization, or conjugation with other functional moieties^[1].

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

Anti-Mouse (CSF1R/CD115) Antibody (AFS98) (directly injecyion, 48 h before MCAo) depletes microglia in aged animals but results in increased neuroinflammation after ischemic stroke^[1].
Anti-Mouse (CSF1R/CD115) Antibody (AFS98) (25 mg/kg, i.p., every second day for 6 weeks) suppresses the progression of established diabetic nephropathy^[2].
in Obese (db/db) mice by targeting macrophage-mediated injury^[2].
Anti-Mouse (CSF1R/CD115) Antibody (AFS98) (2 mg/mouse, i.p., every second day for 6 weeks) acts as protection from early atherogenesis in apoE-deficient mice^[3].
Anti-Mouse (CSF1R/CD115) Antibody (AFS98) (25 or 50 mg/kg, i.p., every day for 14 days) shows significant antiinflammatory effects in Collagen-induced arthritis (CIA) mice models^[4].

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

12978  [NCBI]

P09581

in vivo macrophage depletion; in vitro CSF1R neutralization; in vivo monocyte depletion; Flow cyt

Unconjugated

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

150 kDa

Liquid

Colorless to light yellow

[Anti-Mouse CSF1R/CD115 Antibody (AFS98)]

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

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

• 
  Immobilized CSF1R Protein, Mouse (HEK293, His, HY-P72952) can bind Anti-Mouse CSF1R/CD115 Antibody (AFS98). The EC₅₀ for this effect is 262.9 ng/mL.

• [1]. Marino Lee S, et al. Microglia depletion increase brain injury after acute ischemic stroke in aged mice. Exp Neurol. 2021 Feb;336:113530.  [Content Brief]

  [2]. Lim AK, et al. Antibody blockade of c-fms suppresses the progression of inflammation and injury in early diabetic nephropathy in obese db/db mice. Diabetologia. 2009 Aug;52(8):1669-79.  [Content Brief]

  [3]. Murayama T, et al. Intraperitoneal administration of anti-c-fms monoclonal antibody prevents initial events of atherogenesis but does not reduce the size of advanced lesions in apolipoprotein E-deficient mice. Circulation. 1999 Apr 6;99(13):1740-6.  [Content Brief]

  [4]. Toh ML, et al. Bone- and cartilage-protective effects of a monoclonal antibody against colony-stimulating factor 1 receptor in experimental arthritis. Arthritis Rheumatol. 2014 Nov;66(11):2989-3000.  [Content Brief]