Application of topical minoxidil in acne vulgaris treatment

Abstract Background: Acne vulgaris (AV) results from increased sebum production and Cutibacterium acnes (C. acnes) overgrowth, leading to pilosebaceous unit inflammation. The androgen-androgen receptor (AR) pathway significantly contributes to acne development, with minoxidil showing promise in supp...

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Published inDermatologica Sinica Vol. 42; no. 3; pp. 225 - 235
Main Authors Chen, Chun-Bing, Kuo, Yung-Chia, Chang, Sun-Min, Lin, An-Chi, Fan, Hsien-Chi, Lin, Tung-Liang, Chung, Wen-Hung, Hsu, Cheng-Lung
Format Journal Article
LanguageEnglish
Published India Wolters Kluwer - Medknow 01.07.2024
Medknow Publications and Media Pvt. Ltd
Wolters Kluwer Medknow Publications
Edition2
Subjects
Online AccessGet full text
ISSN1027-8117
2223-330X
DOI10.4103/ds.DS-D-24-00105

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Abstract Abstract Background: Acne vulgaris (AV) results from increased sebum production and Cutibacterium acnes (C. acnes) overgrowth, leading to pilosebaceous unit inflammation. The androgen-androgen receptor (AR) pathway significantly contributes to acne development, with minoxidil showing promise in suppressing AR-related activities. Objectives: This study aims to examine the mechanism and effectiveness of minoxidil in treating AV. Methods: The effects of minoxidil on lipid metabolism and bacterial infection/inflammation were tested. A clinical trial was performed to evaluate the effect of topical minoxidil on AV. Results: Minoxidil suppressed fatty acid synthase activity and lipid formation in an androgen-sensitive prostate cancer cell line in vitro and sebum formation in hamster flank organs in vivo. For C. acnes, minoxidil had a half-maximum inhibitory concentration of 5 mM. Both 2% and 5% minoxidil suppressed C. acnes-induced infection/inflammation in an animal model. A phase I/II clinical trial of topical minoxidil in treating AV using a split-face model demonstrated a good response and well-tolerated side effects. Compared to the untreated side, the numbers of all types of lesions decreased significantly on the treated side on day 3 (mean: −2.238, 95% confidence interval [CI]: −3.821 to −0.655, P = 0.008), day 8, and reached the maximum effect on day 15 (mean: −1.286, 95% CI: −2.151 to −0.420, P = 0.006). Responders to topical minoxidil may experience rapid regression of acne as early as 3 days of treatment. Conclusion: Our collective data indicate that minoxidil could inhibit AR-related functions and C. acnes growth in treating AV.
AbstractList Background: Acne vulgaris (AV) results from increased sebum production and Cutibacterium acnes (C. acnes) overgrowth, leading to pilosebaceous unit inflammation. The androgen-androgen receptor (AR) pathway significantly contributes to acne development, with minoxidil showing promise in suppressing AR-related activities. Objectives: This study aims to examine the mechanism and effectiveness of minoxidil in treating AV. Methods: The effects of minoxidil on lipid metabolism and bacterial infection/inflammation were tested. A clinical trial was performed to evaluate the effect of topical minoxidil on AV. Results: Minoxidil suppressed fatty acid synthase activity and lipid formation in an androgen-sensitive prostate cancer cell line in vitro and sebum formation in hamster flank organs in vivo. For C. acnes, minoxidil had a half-maximum inhibitory concentration of 5 mM. Both 2 and 5 minoxidil suppressed C. acnes-induced infection/inflammation in an animal model. A phase I/II clinical trial of topical minoxidil in treating AV using a split-face model demonstrated a good response and well-tolerated side effects. Compared to the untreated side, the numbers of all types of lesions decreased significantly on the treated side on day 3 (mean: -2.238, 95 confidence interval [CI]: -3.821 to -0.655, P = 0.008), day 8, and reached the maximum effect on day 15 (mean: -1.286, 95 CI: -2.151 to -0.420, P = 0.006). Responders to topical minoxidil may experience rapid regression of acne as early as 3 days of treatment. Conclusion: Our collective data indicate that minoxidil could inhibit AR-related functions and C. acnes growth in treating AV. Keywords: Acne, androgen, androgen receptor, C. acnes, minoxidil
Acne vulgaris (AV) results from increased sebum production and Cutibacterium acnes (C. acnes) overgrowth, leading to pilosebaceous unit inflammation. The androgen-androgen receptor (AR) pathway significantly contributes to acne development, with minoxidil showing promise in suppressing AR-related activities. This study aims to examine the mechanism and effectiveness of minoxidil in treating AV. The effects of minoxidil on lipid metabolism and bacterial infection/inflammation were tested. A clinical trial was performed to evaluate the effect of topical minoxidil on AV. Minoxidil suppressed fatty acid synthase activity and lipid formation in an androgen-sensitive prostate cancer cell line in vitro and sebum formation in hamster flank organs in vivo. For C. acnes, minoxidil had a half-maximum inhibitory concentration of 5 mM. Both 2 and 5 minoxidil suppressed C. acnes-induced infection/inflammation in an animal model. A phase I/II clinical trial of topical minoxidil in treating AV using a split-face model demonstrated a good response and well-tolerated side effects. Compared to the untreated side, the numbers of all types of lesions decreased significantly on the treated side on day 3 (mean: -2.238, 95 confidence interval [CI]: -3.821 to -0.655, P = 0.008), day 8, and reached the maximum effect on day 15 (mean: -1.286, 95 CI: -2.151 to -0.420, P = 0.006). Responders to topical minoxidil may experience rapid regression of acne as early as 3 days of treatment. Our collective data indicate that minoxidil could inhibit AR-related functions and C. acnes growth in treating AV.
Abstract Background: Acne vulgaris (AV) results from increased sebum production and Cutibacterium acnes (C. acnes) overgrowth, leading to pilosebaceous unit inflammation. The androgen-androgen receptor (AR) pathway significantly contributes to acne development, with minoxidil showing promise in suppressing AR-related activities. Objectives: This study aims to examine the mechanism and effectiveness of minoxidil in treating AV. Methods: The effects of minoxidil on lipid metabolism and bacterial infection/inflammation were tested. A clinical trial was performed to evaluate the effect of topical minoxidil on AV. Results: Minoxidil suppressed fatty acid synthase activity and lipid formation in an androgen-sensitive prostate cancer cell line in vitro and sebum formation in hamster flank organs in vivo. For C. acnes, minoxidil had a half-maximum inhibitory concentration of 5 mM. Both 2% and 5% minoxidil suppressed C. acnes-induced infection/inflammation in an animal model. A phase I/II clinical trial of topical minoxidil in treating AV using a split-face model demonstrated a good response and well-tolerated side effects. Compared to the untreated side, the numbers of all types of lesions decreased significantly on the treated side on day 3 (mean: −2.238, 95% confidence interval [CI]: −3.821 to −0.655, P = 0.008), day 8, and reached the maximum effect on day 15 (mean: −1.286, 95% CI: −2.151 to −0.420, P = 0.006). Responders to topical minoxidil may experience rapid regression of acne as early as 3 days of treatment. Conclusion: Our collective data indicate that minoxidil could inhibit AR-related functions and C. acnes growth in treating AV.
Background: Acne vulgaris (AV) results from increased sebum production and Cutibacterium acnes (C. acnes) overgrowth, leading to pilosebaceous unit inflammation. The androgen-androgen receptor (AR) pathway significantly contributes to acne development, with minoxidil showing promise in suppressing AR-related activities. Objectives: This study aims to examine the mechanism and effectiveness of minoxidil in treating AV. Methods: The effects of minoxidil on lipid metabolism and bacterial infection/inflammation were tested. A clinical trial was performed to evaluate the effect of topical minoxidil on AV. Results: Minoxidil suppressed fatty acid synthase activity and lipid formation in an androgen-sensitive prostate cancer cell line in vitro and sebum formation in hamster flank organs in vivo. For C. acnes, minoxidil had a half-maximum inhibitory concentration of 5 mM. Both 2% and 5% minoxidil suppressed C. acnes-induced infection/inflammation in an animal model. A phase I/II clinical trial of topical minoxidil in treating AV using a split-face model demonstrated a good response and well-tolerated side effects. Compared to the untreated side, the numbers of all types of lesions decreased significantly on the treated side on day 3 (mean: −2.238, 95% confidence interval [CI]: −3.821 to −0.655, P = 0.008), day 8, and reached the maximum effect on day 15 (mean: −1.286, 95% CI: −2.151 to −0.420, P = 0.006). Responders to topical minoxidil may experience rapid regression of acne as early as 3 days of treatment. Conclusion: Our collective data indicate that minoxidil could inhibit AR-related functions and C. acnes growth in treating AV.
Audience Academic
Author Kuo, Yung-Chia
Hsu, Cheng-Lung
Chen, Chun-Bing
Chang, Sun-Min
Fan, Hsien-Chi
Lin, Tung-Liang
Lin, An-Chi
Chung, Wen-Hung
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Snippet Abstract Background: Acne vulgaris (AV) results from increased sebum production and Cutibacterium acnes (C. acnes) overgrowth, leading to pilosebaceous unit...
Background: Acne vulgaris (AV) results from increased sebum production and Cutibacterium acnes (C. acnes) overgrowth, leading to pilosebaceous unit...
Acne vulgaris (AV) results from increased sebum production and Cutibacterium acnes (C. acnes) overgrowth, leading to pilosebaceous unit inflammation. The...
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SubjectTerms acne
androgen
androgen receptor
Androgens
Antiacne agents
c. acnes
Drug therapy
Fatty acids
Hamsters
Inflammation
Minoxidil
Original Article
Prostate cancer
Synthesis
Tetracycline
Tetracyclines
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Title Application of topical minoxidil in acne vulgaris treatment
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