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This study found that supplementing soybean oil significantly increased the production of the cyclosporine A derivative [(4'-OH)MeLeu]4-CsA by 55.6%, offering potential enhancements for its clinical application.

This study found that Cyclosporin A may prolong the anagen phase of hair growth in cultured dermal papilla cells by decreasing TGF-β2 expression, similar to its mechanism in immunosuppression.

This study analyzed the structure and dynamics of ketoconazole, revealing how its molecular characteristics, such as spin-lattice relaxation time and chemical shift anisotropy, are influenced by π-π stacking interactions and different carbon site environments.

This study found that applying dexamethasone to mice induced catagen-like follicle changes significantly earlier and more consistently than a vehicle, such changes being useful for studying hair follicle regression.

This study demonstrates that inhibiting SFRP1 with the antagonist WAY-316606 enhances hair growth in human scalp hair follicles ex vivo by facilitating Wnt signalling.

This study found that cyclosporin A treatment enhances hair growth in mice by inhibiting calcineurin-NFAT1 activity, which alters keratinocyte differentiation and apoptosis-related gene expression in hair follicles.

This study found that immune-mediated destruction of bulge stem cells is a key factor in the alopecia observed in AE mice, suggesting it as a model for studying primary cicatricial alopecias, particularly lichen planopilaris.

This study found that topical application of FK506 stimulated hair growth in animals, which may occur independently of its immunosuppressive effects, though its effect on human hair growth remains unclear.

In this study, only 1 out of 5 patients with anti-TNF-α induced psoriasiform eruptions showed good response to topical treatment, while systemic therapy and discontinuation of anti-TNF-α may prevent scarring alopecia in severe cases.

This study found that cyclosporin A stimulates growth in cultured murine hair epithelial cells and reduces protein kinase C expression, suggesting that these actions may contribute to its hair-growing effects.

This study introduces a mouse model of cyclophosphamide-induced alopecia, which effectively replicates human chemotherapy-induced hair loss and can be pharmacologically manipulated to study hair regrowth patterns.

In this study, gene expression profiling in mice identified fluphenazine and iloprost as potential inducers of hair growth, highlighting a new strategy for exploring hair-growth treatments in animal models.

This study found that cyclosporine A may lead to partial hair regrowth in 50% of patients with severe alopecia areata who do not respond to standard treatments.

This study provides evidence that Cyclosporine A inhibits catagen development in human hair follicles, suggesting different underlying mechanisms from those observed in rodent studies.

This study found that cyclosporin A treatment in young nude mice induced dose-dependent hair growth, which stopped after treatment cessation, but did not result in hair growth in older mice.

This study found that both ciclosporin A and topical therapy were effective in reducing alopecia and scaling in dogs with idiopathic sebaceous adenitis, with evidence suggesting improved outcomes when both treatments are combined.

This study found that cyclophosphamide-induced hair follicle damage in C3H mice could be remodelled into intact anagen hair follicles with topical cyclosporin A, especially in anagen IV stage follicles.

This study found that topical cyclosporine significantly prolonged the survival of skin allografts in a rat model, with maximum effectiveness achieved through local direct application.

This study found that regio-specific hydroxylation of cyclosporine A in Sebekia benihana is mediated by the cytochrome P450 hydroxylase CYP-sb21, suggesting potential biotechnological applications for hair growth promotion without immunosuppressive effects.

In this study, cyclosporine A stimulated hair growth in mouse vibrissae organ culture by promoting matrix cell proliferation and altering growth factor expression.

High doses of cyclosporine A increase testosterone conversion, possibly boosting hair growth.

This study found that cyclosporine A's enhancement of hair growth in mice is partly due to its ability to block the nuclear translocation of apoptosis-inducing factor, slowing the hair follicle transition to the catagen phase.

This study concluded that combining systemic cyclosporine A with low-dose corticosteroids effectively treats severe alopecia areata while maintaining safe cyclosporine A levels in the blood.

This study found that cyclosporine-A might significantly increase the risk of cerebral venous and arterial thrombosis in patients with aplastic anemia.

In this study, topical application of Cyclosporin A on mice skin induced hair growth by transitioning follicles from telogen to anagen, but no effect was observed on cultured human hair follicles.

This study found that the cytochrome P450 enzyme CYP-sb21 can hydroxylate cyclosporine A at multiple positions, reducing its immunosuppressive effects but retaining its hair growth-promoting side-effect, and suggests modifications to improve regioselectivity for commercial use.

This study identified a cytochrome P450 enzyme, CYP-pa1 from Pseudonocardia autotrophica, as responsible for the specific hydroxylation of cyclosporin A at the 9th N-methyl leucine, suggesting potential for biotechnological applications.

This case report highlights a severe kidney injury linked to the combined use of ciclosporin and simvastatin in a patient treated for alopecia universalis.

In this case report, the authors highlight a 20-month-old girl with nephrotic syndrome who experienced severe alopecia due to an accidental high dose of cyclosporine; her hair regrew after the drug was stopped.

This case report describes a patient with hemophagocytic lymphohistiocytosis who developed hypertrichosis and eyelash trichomegaly, likely linked to cyclosporine-A and prednisolone therapy, with expected resolution after stopping treatment.