TNF-α
Pro-inflammatory cytokine central to the NF-κB signalling cascade; principal downstream readout in anti-inflammatory peptide research.
For laboratory and research use only — not for human consumption.
Tumour necrosis factor alpha (TNF-α) is a 17 kDa homotrimeric cytokine produced primarily by activated macrophages and T-cells that plays a central role in acute and chronic inflammation, immune regulation, and apoptosis. It signals through two distinct receptors — TNFR1 (ubiquitously expressed) and TNFR2 (predominantly on immune cells and endothelium) — activating downstream NF-κB, MAPK, and JNK pathways that drive expression of additional pro-inflammatory cytokines (IL-6, IL-1β), adhesion molecules, and matrix metalloproteinases. Sustained TNF-α elevation is a feature of inflammatory bowel disease, rheumatoid arthritis, psoriasis, and many chronic inflammatory conditions — the mechanistic rationale for anti-TNF-α biologics (infliximab, adalimumab, etanercept) that have transformed autoimmune-disease treatment. In peptide research, TNF-α concentration is the principal downstream endpoint for compounds targeting NF-κB pathway suppression: KPV directly suppresses NF-κB-driven TNF-α transcription; BPC-157 attenuates TNF-α in colitis and muscle-injury models; thymosin-derived compounds reduce TNF-α in LPS-stimulated macrophages. Quantification by ELISA or Luminex multiplex in cell-culture supernatants or tissue lysates is standard.