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替拉瑞林治疗光化性角化病的概况

Profile of Tirbanibulin for the Treatment of Actinic Keratosis.

作者信息

Berman Brian, Grada Ayman, Berman Daniela K

机构信息

Dr. B. Berman is with the Department of Dermatology and Cutaneous Surgery at the University of Miami Miller School of Medicine in Miami, Florida, and the Center for Clinical and Cosmetic Research in Aventura, Florida.

Dr. Grada is with the Department of Dermatology at Case Western Reserve University School of Medicine in Cleveland, Ohio.

出版信息

J Clin Aesthet Dermatol. 2022 Oct;15(10 Suppl 1):S3-S10.

PMID:36408375
原文链接:https://pmc.ncbi.nlm.nih.gov/articles/PMC9586524/
Abstract

Actinic keratosis (AK) is a chronic disease resulting from deleterious effects of long-term, cumulative, epidermal exposure to ultraviolet (UV) light. UV-induced mutations in p53, ras, and p16 genes lead to the emergence of abnormal epidermal actinic keratosis (AKs) cells, which proliferate while avoiding apoptosis and may lead to invasive squamous cell carcinoma. There are both lesion-targeted and field-directed topical treatments. This review is of new and emerging information on tirbanibulin and tirbanibulin 1% ointment, which is approved for topical field treatment of actinic keratosis on the face and scalp. Potent antiproliferative and proapoptotic activities result from tirbanibulin's inhibition tubulin polymerization and disruption of microtubule formation and Src kinase signaling. Tirbanibulin 1% ointment is an effective treatment of facial and scalp AK after five consecutive once-daily applications, as measured by complete and partial clearance and percent reduction in the number of lesions. Localized skin reactions are usually mild to moderate, resolving within a month. The short and well-tolerated course of therapy results in very high patient adherence to the treatment regimen.

摘要

光化性角化病(AK)是一种慢性疾病,由长期累积的表皮暴露于紫外线(UV)的有害影响所致。紫外线诱导的p53、ras和p16基因中的突变导致异常的表皮光化性角化病(AK)细胞出现,这些细胞增殖同时避免凋亡,并可能导致侵袭性鳞状细胞癌。有针对病变的和针对区域的局部治疗方法。本综述介绍了关于替尔泊肽和1%替尔泊肽软膏的新出现的信息,该软膏已被批准用于面部和头皮光化性角化病的局部区域治疗。替尔泊肽抑制微管蛋白聚合、破坏微管形成和Src激酶信号传导,从而产生强大的抗增殖和促凋亡活性。通过完全和部分清除以及病变数量减少百分比来衡量,连续每日一次应用五次后,1%替尔泊肽软膏是治疗面部和头皮AK的有效方法。局部皮肤反应通常为轻度至中度,在一个月内消退。疗程短且耐受性良好,导致患者对治疗方案的依从性非常高。

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Topical Treatments for Basal Cell Carcinoma and Actinic Keratosis in the United States.美国基底细胞癌和光化性角化病的局部治疗方法
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本文引用的文献

1
Commentary: Complete Clearance of Actinic Keratosis with Tirbanibulin Ointment 1% is not Correlated with the Severity of Local Skin Reactions.评论:1%替拉尼布林软膏完全清除光化性角化病与局部皮肤反应的严重程度无关。
J Clin Aesthet Dermatol. 2022 Oct;15(10 Suppl 1):S13-S14.
2
Focused update: Guidelines of care for the management of actinic keratosis.聚焦更新:光化性角化病管理指南。
J Am Acad Dermatol. 2022 Aug;87(2):373-374.e5. doi: 10.1016/j.jaad.2022.04.013. Epub 2022 Apr 18.
3
Topical tirbanibulin eradication of periungual squamous cell carcinoma.外用替巴尼布林根除甲周鳞状细胞癌。
JAAD Case Rep. 2021 Jun 26;14:101-103. doi: 10.1016/j.jdcr.2021.06.013. eCollection 2021 Aug.
4
Guidelines of care for the management of actinic keratosis.光化性角化病治疗管理指南。
J Am Acad Dermatol. 2021 Oct;85(4):e209-e233. doi: 10.1016/j.jaad.2021.02.082. Epub 2021 Apr 2.
5
Ten-Year Follow-up of Persons With Sun-Damaged Skin Associated With Subsequent Development of Cutaneous Squamous Cell Carcinoma.日光性皮肤损伤与随后发生的皮肤鳞状细胞癌的 10 年随访。
JAMA Dermatol. 2021 May 1;157(5):559-565. doi: 10.1001/jamadermatol.2021.0372.
6
Frequency of procedural and medical treatments of actinic keratosis.光化性角化病的手术及药物治疗频率
J Am Acad Dermatol. 2022 Apr;86(4):916-918. doi: 10.1016/j.jaad.2021.03.047. Epub 2021 Mar 20.
7
Phase 3 Trials of Tirbanibulin Ointment for Actinic Keratosis.三期临床试验研究替比嘧啶软膏治疗光化性角化病。
N Engl J Med. 2021 Feb 11;384(6):512-520. doi: 10.1056/NEJMoa2024040.
8
Patient-reported outcomes of topical therapies in actinic keratosis: A systematic review.光化性角化病局部治疗的患者报告结局:系统评价。
Dermatol Ther. 2021 Mar;34(2):e14833. doi: 10.1111/dth.14833. Epub 2021 Feb 21.
9
The Genomic Landscape of Actinic Keratosis.光化性角化病的基因组全景
J Invest Dermatol. 2021 Jul;141(7):1664-1674.e7. doi: 10.1016/j.jid.2020.12.024. Epub 2021 Jan 19.
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Reversible binding of the anticancer drug KXO1 (tirbanibulin) to the colchicine-binding site of β-tubulin explains KXO1's low clinical toxicity.抗癌药物 KXO1(曲贝替定)与β-微管蛋白秋水仙碱结合位点的可逆结合解释了 KXO1 临床毒性低的原因。
J Biol Chem. 2019 Nov 29;294(48):18099-18108. doi: 10.1074/jbc.RA119.010732. Epub 2019 Oct 18.