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Drug Targeting to the Lung: Chemical and Biochemical Considerations
Published in Anthony J. Hickey, Sandro R.P. da Rocha, Pharmaceutical Inhalation Aerosol Technology, 2019
Peter A. Crooks, Narsimha R. Penthala, Abeer M. Al-Ghananeem
These agents may be useful in platelet activating factor-induced bronchoconstriction (Kasperska-Zajac et al. 2008). In the hetrazepine class of platelet activating factor antagonist, apafant (WEB-2086) (44) has been shown to be rapidly absorbed following oral administration and produced no significant adverse effects (Jacobs et al. 1992). Two other compounds—WEB-2347 (45) and E-6123 (46)—also from the hetrazepine class, have emerged as orally active derivatives with profiles superior to WEB-2086 (44).
Development of a Novel IgG1 Anaphylaxis Mouse Model with Uniquely Characteristic Skin Manifestations Induced Through the FcγRIII-Histamine Pathway
Published in Immunological Investigations, 2023
Masato Terashi, Kouya Yamaki, Yutaka Koyama
In a previous study, it was reported that hypothermia due to IgG1 anaphylaxis could be suppressed by administering a PAF receptor antagonist (Jiao et al. 2014; Tsujimura et al. 2008). In our model, we administered Apafant, a PAF receptor antagonist, to examine the effects of PAF, but it did not suppress anaphylactic symptoms and G-ASDIS (Figure 2b). This reinforces the unimportance of PAF in our model. In our IgG1 anaphylaxis model, hypothermia, and G-ASDIS were improved with the administration of the histamine receptor antagonist, levocetirizine (Figure 2a), indicating that histamine, not PAF, is important. The anaphylatoxin C3a degranulates mast cells and basophils and has vasodilatory effects (Klos et al. 2009; Schäfer et al. 2013). However, anaphylatoxin in mice is not considered to be important in the PSA model (Strait et al. 2002). Similarly, in our IgG1 anaphylaxis model, the C3a receptor antagonist did not inhibit the decrease in body temperature (Figure 2C), suggesting that it was not an important factor.