• PN: B111164


45x Ab-conjugated beads (S4P5 - human IL-23 Ab-bead). PN: B111164A. One vial containing 100 µL of anti-human IL-23p40 conjugated to AimPlex Bead S4P5.

25x Biotin-detection Ab (human IL-23p19 Biotin-dAb).PN: B111164B. One vial containing 100 µL of biotinylated anti-human IL-23p19.

Lyophilized Standard Mix-Human Group 3 Panel B, 12-Plex. PN: HG3012B. One vial containing lyophilized recombinant human IL-9, IL-15, IL-16, IL-17C, IL-23p19, IL-24, IL-27, IL-31, IL-32, IL-34, OSM, and SCF.  Note: If multiple analyte kits on the above target list are ordered as a panel, only one vial of standard mix is supplied for those analyte kits.

STORAGE:  2-8 C in the dark.

IMPORTANT: Sodium azide forms explosive compounds with heavy metals. These products contain <0.05% (w/w) azide which with repeated contact with lead and copper commonly found in plumbing drains may result in the buildup of shock sensitive compounds. Dispose in accordance with regulations from your institute.

APPLICATION: Optimal antibody pair and antigen standard for assaying human IL-23p19.  Can be multiplexed with other analytes in Human Group 3.  To be used in conjunction with the AimPlex NR Basic Kit (PN: P100001) and a diluent kit. Refer to the AimPlex Multiplex Immunoassay User Manual and kit inserts for the assay procedure.

For Research Use Only.  Not for use in diagnostic procedures.

Assay Specifications:

Sample types: Cell culture supernatant, serum, plasma, bodily fluid and tissue/cell lysate

Sensitivity (LOD): < 5 pg/mL

Quantitation range:

LLOQ: < 10 pg/mL

ULOQ: > 5,000 pg/mL

Standard dose recovery: 70-130%

Intra-assay CV: < 10%

Inter-assay CV: < 20%

Cross-reactivity of analytes in Human Group 3: Negligible

Sample volume: 15 µL/test


Interleukin-23 (IL-23) also known as IL-23 alpha subunit p19 (IL-23p19 or IL-23A), is a heterodimeric cytokine composed of an IL-12p40 subunit that is shared with IL-12 and the IL-23p19 subunit. Prior to the discovery of IL-23, IL-12 had been proposed to represent a key mediator of inflammation in mouse models of inflammation. However, many studies aimed at assessing the role of IL-12 had blocked the activity of IL-12p40, and were therefore not as specific as thought. Studies which blocked the function of IL-12p35 did not produce the same results as those targeting IL-12p40 as would have been expected if both subunits formed part of IL-12 only. Seminal studies in experimental autoimmune encephalomyelitis, a mouse model of multiple sclerosis, showed that IL-23 was responsible for the inflammation observed. IL-23 has shown to facilitate development of inflammation in numerous other models of immune pathology where IL-12 had previously been implicated including models of arthritis, intestinal inflammation, and psoriasis. Diseases associated with IL23A include colitis.


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