Experimental allergic encephalitogenic peptide (human), an EAE peptide, induces encephalomyelitis in guinea pigs [1].

NPC 567 acetate is a bradykinin B2 antagonist and can be used in studies about the treatment of allergic airway disease.

Lyn peptide inhibitor acetate is a potent and cell-permeable inhibitor of Lyn-coupled IL-5 receptor signaling pathway, while keeping other signals intact. Lyn peptide inhibitor blocks Lyn activation and inhibits the binding of Lyn tyrosine kinase to βc subunit of IL-3/GM-CSF/IL-5 receptors. Lyn peptide inhibitor can be used for study of asthma, allergic, and other eosinophilic disorders.

C5a Anaphylatoxin (human) is a pro-inflammatory peptide that functions as a leukocyte chemoattractant, utilized in researching inflammation and immune responses, including allergic asthma [1] [2].

CKLF1-C19, the C-terminal peptide of human chemokine-like factor 1 (CKLF1), interacts with CCR4 and inhibits chemotaxis induced by CKLF1 and CCL17. It also suppresses allergic lung inflammation by inhibiting chemotaxis mediated by CCR3 and CCR4 [1].

Lyn Peptide Inhibitor TFA is a powerful, cell-permeable inhibitor specifically targeting the Lyn-coupled IL-5 receptor signaling pathway, without affecting alternative signaling pathways. It effectively prevents Lyn activation and impedes the association between Lyn tyrosine kinase and the βc subunit of IL-3/GM-CSF/IL-5 receptors. This compound is utilized in the investigation of asthma, allergic reactions, and various eosinophilic conditions [1].

EPI-X4, an endogenous peptide fragment of human serum albumin (amino acids 408-423), serves as an antagonist to the chemokine (C-X-C motif) receptor 4 (CXCR4). It effectively prevents calcium mobilization and receptor internalization triggered by chemokine (C-X-C motif) ligand 12 (CXCL12) in HEK293 cells with CXCR4 expression, at concentrations between 0.8 and 1,000 µM. Moreover, EPI-X4 hampers the CXCL12-driven migration of both Jurkat T cells and human CD34+ hematopoietic stem cells. In an acute allergic airway hypereosinophilia mouse model, EPI-X4 intrinsically decreases Cxcr4-dependent inflammatory cell infiltration in airways at a dose of 16 µmol/kg. Additionally, increased urinary EPI-X4 levels, inversely related to glomerular filtration rate (GFR), are observed in chronic kidney disease patients, indicating its potential biomarker role.

FIZZ-1 (32-51) (mouse), a cysteine-rich secretory protein, is predominantly expressed in macrophages, bronchial epithelial, and type II alveolar epithelial cells (AEC) during allergic airway inflammation. Additionally, it exhibits an anti-apoptotic effect on lung fibroblasts, indicating its potential utility in researching allergic pneumonia [1] [2].