ArthritoMab™ Antibody Cocktail for C57BL/6, 50 mg

ArthritoMab™ Antibody Cocktail is a reformulated cocktail of 4 monoclonal antibodies for the induction of arthritis as an alternative to the widely used collagen-induced arthritis (CIA) model. Many transgenic strains of...

Antibodies

CIA-MAB-2C

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For research use only. Not for use in diagnostic procedures.

ArthritoMab™ Antibody Cocktail is a reformulated cocktail of 4 monoclonal antibodies for the induction of arthritis as an alternative to the widely used collagen-induced arthritis (CIA) model. Many transgenic strains of mice are on a C57BL/6 background. However this strain is refractory to arthritis induction either by CIA or CAIA. Traditionally to overcome this in the CAIA model an increased dose of antibody cocktail is given. This reformulated cocktail of antibodies is optimized for production of arthritis in C57BL/6, inducing arthritis with lower doses of antibody. This new formulation can also be used in other strains of mouse, which traditionally require greater amounts of cocktail.

The Collagen Antibody Induced Arthritis (CAIA) model is a relevant model for studying the efferent phase of RA, where leukocytes are attracted and respond to the immune complex in the joint. It is induced using a cocktail of antibodies to anti-CII and contains pathogenic features similar to that of RA such as pannus formation, cellular infiltration, synovitis and cartilage/bone destruction.

Download the whitepaper. 

 

Benefits of the CAIA model

  • Length of study: Arthritis develops in mice typically within 24-48 hr allowing the completion of a study within 2 weeks reducing the number of assessments and scoring periods.
  • Reduced group size: Rate of incidence is nearly 100% depending on the strain allowing for smaller group sizes.
  • Synchronization: onset of disease is synchronized between animals simplifying treatment schedules.
  • Steady & Controlled disease progression: No rapid & severe disease spikes enabling evaluation of all treatment schedules
  • Susceptibility: Induce arthritis in transgenic strains with as little as 2 mg of Antibody. 

 

Comparison

 

ArthritoMab™

Competitor

Epitopes Recognized

CB11, CB10, CB8

CB11 only

Disease Progression

Steady & Controlled

Rapid & Severe

Paw involvement

Consistent & Predominantely rear

Variable & unpredictable

Amount required for C57Bl/6

2 mg (25 animals per vial)

5 mg (8 animals per vial)

 

Abreviations:

  • Anti-Collagen Induced arthritis (ACIA)
  • Monoclonal Antibody induced arthritis (mAb-RA)
  • Collagen Antibody Induced Arthritis (CAIA)

 

References/Citations:

Sangaletti, S., Botti, L., Gulino, A., Lecis, D., Bassani, B., Portararo, P., ... & Colombo, M. P. (2020). SPARC regulation of PMN clearance protects from pristane induced lupus and rheumatoid arthritis. Available at SSRN 3678911.

Nandakumar, K. S., Collin, M., Happonen, K. E., Lundström, S. L., Croxford, A. M., Xu, B., ... & Holmdahl, R. (2018). Streptococcal endo--N-acetylglucosaminidase suppresses antibody mediated inflammation in vivo. Frontiers in immunology, 9, 1623.

Hamamura, K., Nishimura, A., Chen, A., Takigawa, S., Sudo, A., & Yokota, H. (2015). Salubrinal acts as a Dusp2 inhibitor and suppresses inflammation in anti-collagen antibody-induced arthritis. Cellular signalling, 27(4), 828-835

Asnagli, H., Martire, D., Belmonte, N., Quentin, J., Bastian, H., Boucard-Jourdin, M., ... & Marchetti, I. (2014). Type 1 regulatory T cells specific for collagen type II as an efficient cell-based therapy in arthritis. Arthritis research & therapy, 16(3), R115

Ohtsubo-Yoshioka, M., Nunomura, S., Kataoka, T. R., Okayama, Y., & Ra, C. (2013). Fc receptor beta chain deficiency exacerbates murine arthritis in the anti-type II collagen antibody-induced experimental model. Modern rheumatology, 23(4), 804-810

Leavenworth, J. W., Tang, X., Kim, H. J., Wang, X., & Cantor, H. (2013). Amelioration of arthritis through mobilization of peptide-specific CD8+ regulatory T cells. The Journal of clinical investigation, 123(3), 1382-1389.

Jacques, P., Lambrecht, S., Verheugen, E., Pauwels, E., Kollias, G., Armaka, M., ... & Elewaut, D. (2013). Proof of concept: enthesitis and new bone formation in spondyloarthritis are driven by mechanical strain and stromal cells. Annals of the rheumatic diseases, annrheumdis-2013

Kudryavtseva, E., Forde, T. S., Pucker, A. D., & Adarichev, V. A. (2012). Wnt signaling genes of murine chromosome 15 are involved in sex‐affected pathways of inflammatory arthritis. Arthritis & Rheumatism, 64(4), 1057-1068

Te Boekhorst, B. C., Jensen, L. B., Colombo, S., Varkouhi, A. K., Schiffelers, R. M., Lammers, T., ... & Nicolay, K. (2012). MRI-assessed therapeutic effects of locally administered PLGA nanoparticles loaded with anti-inflammatory siRNA in a murine arthritis model. Journal of controlled release, 161(3), 772-780.

Dimitrova, P., Ivanovska, N., Belenska, L., Milanova, V., Schwaeble, W., & Stover, C. (2012). Abrogated RANKL expression in properdin-deficient mice is associated with better outcome from collagen-antibody-induced arthritis. Arthritis research & therapy, 14(4), R173.

Wruck, C. J., Fragoulis, A., Gurzynski, A., Brandenburg, L. O., Kan, Y. W., Chan, K., ... & Pufe, T. (2010). Role of oxidative stress in rheumatoid arthritis: insights from the Nrf2-knockout mice. Annals of the rheumatic diseases, annrheumdis132720.



Product Insert (PDF) - Informational use only. Please refer to insert included with product.

Download the whitepaper

Data/Specifications:

Epitope Specificity

The classic CIA model is mediated by autoantibodies which bind to type II collagen and complement. In mice as well as human RA patients, the antibody response that best correlates with disease is directed against the C1, J1 and U1 epitopes. The ArthritoMab™ arthritogenic cocktail of 4 monoclonal antibodies binds to these well-defined epitopes C11b, J1, D3 and U1, which are spread over the entire CII (CB8, CB10 and CB11 fragments). This possibly encourages better immune complex formation on the cartilage surface for the initiation of arthritis and produces consistent and predictable disease in all 4 paws (with predominance for the rear). Competitor products only recognize CB11, which produces variable disease that can contribute to unpredictable involvement in the paws (sometimes more front paw involvement and other times more rear involvement).

Susceptibility

  • Balb/c
  • DBA/1
  • B10.RIII
  • C57Bl/6

Disease Progression & Positive Controls

Disease progression is steady and controlled using ArthritoMab™ antibody cocktail, enabling investigators to evaluate various regimes. Data below was generated using Vehicle, Dexamethasone and Enbrel in the Balb/c strain (induced with 2 mg ArthritoMab™ on day 0 followed by LPS boost on day 3).