Psoriasis Research Reagents

Psoriasis is a chronic, immune-mediated inflammatory skin disease affecting 2–3% of the global population, characterized by keratinocyte hyperproliferation, epidermal thickening, and erythematous scaly plaques. The IL-23/Th17 axis is the central pathogenic pathway: dendritic cell-derived IL-23 drives Th17 cell expansion and IL-17A/F production, which in turn activates keratinocytes and sustains the inflammatory cycle. Biologic therapies have achieved unprecedented skin clearance rates — anti-IL-17A (secukinumab, ixekizumab), anti-IL-17A/F (bimekizumab), anti-IL-23 p19 (guselkumab, risankizumab, tildrakizumab, mirikizumab), anti-IL-12/23 p40 (ustekinumab), and anti-TNF-α (adalimumab, infliximab). TYK2 inhibition (deucravacitinib) represents a new oral mechanism targeting IL-23/IFN signaling.

Research Use Only (RUO)Not intended for diagnostic or therapeutic procedures.

Psoriasis Research Reagents — key pathogenic pathways including IL-23/Th17 axis, IL-17A-driven keratinocyte activation, TNF-alpha amplification, and biologic targets

Fig. 1 Key pathogenic pathways and research targets in psoriasis. DC-derived IL-23 drives Th17 expansion; IL-17A/F activates keratinocyte hyperproliferation; TNF-α amplifies inflammation via NF-κB. Key biologic targets highlighted in orange.

abinScience provides validated reference antibodies, anti-drug antibodies, and ADA ELISA kits covering all major psoriasis biologics — including dedicated ADA toolkits for secukinumab, ixekizumab, and bimekizumab, plus the broadest IL-23 p19 inhibitor panel available (guselkumab, risankizumab, tildrakizumab, mirikizumab, brazikumab). All products are manufactured by our parent company AtaGenix Laboratories under ISO quality systems. Browse products below or contact us for custom antibody development.

Key Research Targets

IL-17A / IL-17A/F — IL-17A is the key effector cytokine driving keratinocyte hyperproliferation, antimicrobial peptide expression, and neutrophil recruitment in psoriatic lesions. Anti-IL-17A biologics (secukinumab, ixekizumab) and anti-IL-17A/F dual inhibitors (bimekizumab) have achieved the highest skin clearance rates in clinical trials. abinScience offers ADA toolkits for all three: reference antibodies, drug-level ELISA kits, anti-drug antibodies (neutralizing and non-neutralizing clones), and neutralizing antibody ELISA kits.
→ Browse IL-17A antibodies, proteins & ELISA kits

IL-23 (p19) — IL-23 is the upstream master regulator of the Th17 pathway. Selective IL-23 p19 inhibitors (guselkumab, risankizumab, tildrakizumab, mirikizumab) achieve durable PASI 90/100 clearance with infrequent dosing. abinScience offers the broadest anti-IL-23 p19 reference antibody panel available, including brazikumab, plus ADA ELISA kits for risankizumab. Anti-IL-12/23 p40 reference antibodies (ustekinumab, briakinumab) are also available.
→ Browse IL-23 antibodies, proteins & ELISA kits

TNF-α — TNF-α amplifies psoriatic inflammation via NF-κB activation and synergizes with IL-17A to sustain keratinocyte activation. Although newer IL-17 and IL-23 inhibitors show superior efficacy, anti-TNF-α agents (adalimumab, infliximab, etanercept) remain widely used, particularly for psoriatic arthritis. Anti-TNF-α reference antibodies, recombinant proteins, and complete ADA ELISA toolkits support biosimilar characterization and TDM research.
→ Browse TNF-α antibodies, proteins & ELISA kits

IL-12/23 p40 — The shared p40 subunit of IL-12 and IL-23 is the target of ustekinumab, the first biologic to demonstrate the importance of the IL-23/Th17 axis in psoriasis. Anti-IL-12/23 p40 reference antibodies (ustekinumab, briakinumab, ebdarokimab) and ADA ELISA kits support mechanism-of-action studies and immunogenicity monitoring. Comparing p40-targeted vs p19-selective approaches is a key research question in psoriasis biologics development.
→ Browse IL-12/23 p40 antibodies & ELISA kits

References

1. Armstrong AW, et al. Pathophysiology, clinical presentation, and treatment of psoriasis: a review. JAMA. 2020;323(19):1945-1960. DOI

2. Gordon KB, et al. Bimekizumab vs secukinumab in plaque psoriasis. N Engl J Med. 2021;385(2):142-152. DOI

3. Nestle FO, et al. Psoriasis. N Engl J Med. 2009;361(5):496-509. DOI