Bayer AG, Berlin, Germany.
Centre for Human Drug Research, Leiden, The Netherlands.
Clin Transl Sci. 2024 Mar;17(3):e13771. doi: 10.1111/cts.13771.
This study evaluated and characterized the pharmacological activity of the orally administered interleukin-1 receptor-associated kinase 4 (IRAK4) inhibitors BAY1834845 (zabedosertib) and BAY1830839 in healthy male volunteers. Participants received one of either IRAK4 inhibitors or a control treatment (prednisolone 20 mg or placebo) twice daily for 7 days. Localized skin inflammation was induced by topical application of imiquimod (IMQ) cream for 3 days, starting at Day 3 of treatment. The inflammatory response was evaluated by laser speckle contrast imaging (skin perfusion) and multispectral imaging (erythema). At Day 7, participants received 1 ng/kg intravenous lipopolysaccharide (LPS). Circulating inflammatory proteins, leukocyte differentiation, acute phase proteins, and clinical parameters were evaluated before and after the systemic LPS challenge. Treatment with BAY1834845 significantly reduced the mean IMQ-induced skin perfusion response (geometric mean ratio [GMR] vs. placebo: 0.69 for BAY1834845, 0.70 for prednisolone; both p < 0.05). Treatment with BAY1834845 and BAY1830839 significantly reduced IMQ-induced erythema (GMR vs. placebo: 0.75 and 0.83, respectively, both p < 0.05; 0.86 for prednisolone, not significant). Both IRAK4 inhibitors significantly suppressed the serum TNF-α and IL-6 responses (≥80% suppression vs. placebo, p < 0.05) and inhibited C-reactive protein, procalcitonin, and IL-8 responses to intravenous LPS. This study demonstrated the pharmacological effectiveness of BAY1834845 and BAY1830839 in suppressing systemically and locally induced inflammatory responses in the same range as prednisolone, underlining the potential value of these IRAK4 inhibitors as future therapies for dermatological or other immune-mediated inflammatory diseases.
本研究评估并描述了口服白细胞介素-1 受体相关激酶 4(IRAK4)抑制剂 BAY1834845(扎贝司特)和 BAY1830839 在健康男性志愿者中的药理学活性。参与者接受 IRAK4 抑制剂或对照治疗(泼尼松龙 20mg 或安慰剂),每天两次,共 7 天。从治疗第 3 天开始,通过涂抹咪喹莫特(IMQ)乳膏诱导局部皮肤炎症,持续 3 天。通过激光散斑对比成像(皮肤灌注)和多光谱成像(红斑)评估炎症反应。在第 7 天,参与者接受 1ng/kg 静脉内脂多糖(LPS)。在全身 LPS 挑战前后评估循环炎症蛋白、白细胞分化、急性期蛋白和临床参数。与安慰剂相比,BAY1834845 治疗显著降低了 IMQ 诱导的皮肤灌注反应的平均值(几何均数比[GMR]:BAY1834845 为 0.69,泼尼松龙为 0.70;均 p<0.05)。BAY1834845 和 BAY1830839 治疗显著降低了 IMQ 诱导的红斑(GMR 与安慰剂相比:分别为 0.75 和 0.83,均 p<0.05;泼尼松龙为 0.86,无统计学意义)。两种 IRAK4 抑制剂均显著抑制血清 TNF-α和 IL-6 反应(与安慰剂相比,抑制率≥80%,p<0.05),并抑制 CRP、降钙素原和 IL-8 对静脉内 LPS 的反应。本研究证明了 BAY1834845 和 BAY1830839 在抑制全身和局部诱导的炎症反应方面的药效学有效性,与泼尼松龙的效果相当,这突出了这些 IRAK4 抑制剂作为未来治疗皮肤科或其他免疫介导的炎症性疾病的潜在价值。