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At least 19 recordsLinked to original sources
PubMed2002

A randomized clinical trial of 5% topical minoxidil versus 2% topical minoxidil and placebo in the treatment of androgenetic alopecia in men.

BACKGROUND: Topical minoxidil solution 2% stimulates new hair growth and helps stop the loss of hair in individuals with androgenetic alopecia (AGA). Results can be variable, and historical experience suggests that higher concentrations of topical minoxidil may enhance efficacy. OBJECTIVE: The purpose of this 48-week, double-blind, placebo-controlled, randomized, multicenter trial was to compare 5% topical minoxidil with 2% topical minoxidil and placebo in the treatment of men with AGA. METHODS: A total of 393 men (18-49 years old) with AGA applied 5% topical minoxidil solution (n = 157), 2% topical minoxidil solution (n = 158), or placebo (vehicle for 5% solution; n = 78) twice daily. Efficacy was evaluated by scalp target area hair counts and patient and investigator assessments of change in scalp coverage and benefit of treatment. RESULTS: After 48 weeks of therapy, 5% topical minoxidil was significantly superior to 2% topical minoxidil and placebo in terms of change from baseline in nonvellus hair count, patient rating of scalp coverage and treatment benefit, and investigator rating of scalp coverage. Hair count data indicate that response to treatment occurred earlier with 5% compared with 2% topical minoxidil. Additionally, data from a patient questionnaire on quality of life, global benefit, hair growth, and hair styling demonstrated that 5% topical minoxidil helped improve patients' psychosocial perceptions of hair loss. An increased occurrence of pruritus and local irritation was observed with 5% topical minoxidil compared with 2% topical minoxidil. CONCLUSION: In men with AGA, 5% topical minoxidil was clearly superior to 2% topical minoxidil and placebo in increasing hair regrowth, and the magnitude of its effect was marked (45% more hair regrowth than 2% topical minoxidil at week 48). Men who used 5% topical minoxidil also had an earlier response to treatment than those who used 2% topical minoxidil. Psychosocial perceptions of hair loss in men with AGA were also improved. Topical minoxidil (5% and 2%) was well tolerated by the men in this trial without evidence of systemic effects.

Administration, Topical↗
PubMed1994

The same enzymes catalyze sulfation of minoxidil, minoxidil analogs and catecholamines.

Rat liver sulfation of minoxidil and minoxidil analogs is described and the enzymes responsible are compared with those that sulfate catecholamines. Our study of minoxidil sulfation showed male-dominant sex dimorphism of the enzyme activity due to two enzymes that coelute with dopamine sulfotransferases. The most abundant isoform, in our routine assay, is minoxidil sulfotransferase 2 (P2). Sulfation ability by this enzyme parallels minoxidil analog antihypertensive ability. Minoxidil, analog and dopamine sulfotransferases were not separable by several different chromatographic methods, supporting their identity. The minoxidil sulfotransferase activity dropped in hypophysectomized males, due mostly to diminished levels of minoxidil sulfotransferase 2/dopamine sulfotransferase II, which appears to be aryl sulfotransferase IV. Its relationship to the minoxidil sulfotransferase reported by the Falany group is not clear. Here, we describe the exploration of rat liver sulfation of antihypertensive minoxidil (2,4-diamino-6-piperidinopyrimidine-3-oxide), and several minoxidil analogs. Minoxidil sulfation was first reported in rat and human liver cytosol by Johnson's group at Upjohn [1,2]. Our interest in the sulfation process arose because direct action of minoxidil sulfate had been implicated both in vivo [3,4] and in vitro [5] in blood pressure control processes.

Animals↗
PubMed2001

Minoxidil-induced hair growth is mediated by adenosine in cultured dermal papilla cells: possible involvement of sulfonylurea receptor 2B as a target of minoxidil.

The mechanism by which minoxidil, an adenosine-triphosphate-sensitive potassium channel opener, induces hypertrichosis remains to be elucidated. Minoxidil has been reported to stimulate the production of vascular endothelial growth factor, a possible promoter of hair growth, in cultured dermal papilla cells. The mechanism of production of vascular endothelial growth factor remains unclear, however. We hypothesize that adenosine serves as a mediator of vascular endothelial growth factor production. Minoxidil-induced increases in levels of intracellular Ca(2+) and vascular endothelial growth factor production in cultured dermal papilla cells were found to be inhibited by 8-sulfophenyl theophylline, a specific antagonist for adenosine receptors, suggesting that dermal papilla cells possess adenosine receptors and sulfonylurea receptors, the latter of which is a well-known target receptor for adenosine-triphosphate-sensitive potassium channel openers. The expression of sulfonylurea receptor 2B and of the adenosine A1, A2A, and A2B receptors was detected in dermal papilla cells by means of reverse transcription polymerase chain reaction analysis. In order to determine which of the adenosine receptor subtypes contribute to minoxidil-induced hair growth, the effects of subtype-specific antagonists for adenosine receptors were investigated. Significant inhibition in increase in intracellular calcium level by minoxidil or adenosine was observed as the result of pretreatment with 8-cyclopentyl-1,3-dipropylxanthine, an antagonist for adenosine A1 receptor, but not by 3,7-dimethyl-1-propargyl-xanthine, an antagonist for adenosine A2 receptor, whereas vascular endothelial growth factor production was blocked by both adenosine A1 and A2 receptor antagonists. These results indicate that the effect of minoxidil is mediated by adenosine, which triggers intracellular signal transduction via both adenosine A1 and A2 receptors, and that the expression of sulfonylurea receptor 2B in dermal papilla cells might play a role in the production of adenosine.

ATP-Binding Cassette Transporters↗
PubMed1994

Stimulation of Cl conductance by minoxidil sulfate and K conductance by minoxidil in eccrine clear cells.

Minoxidil sulfate (MXS), an antihypertensive agent and hair growth promoter, has been reported to stimulate K channels in vascular smooth muscle cells. We now report that MXS stimulates whole cell Cl currents, whereas minoxidil (MX) stimulates K currents in dissociated eccrine clear cells. Using whole cell clamp techniques we observed that: 1) 1 mM MXS stimulated sweat secretion in vitro; 2) MXS depolarized the membrane potential by as much as 40 mV; 3) MXS stimulated membrane conductance, increased inward current and shifted the reversal potential to the right when physiological electrolyte solutions were used; 4) in symmetrical Cl (Cl/Cl) solutions without permeable cations, MXS induced outwardly rectifying current-voltage (I-V) relationships; 5) in the Cl/Cl solutions, the MXS-induced current responses to imposed voltage pulses showed time-dependent activation, especially at the depolarizing potentials; 6) the reversal potential of the MXS-stimulated I-V curves in the Cl/Cl solutions shifted to the right by 55 mV when [Cl] in the bath was decreased from 157 to 7 mM; 7) MXS did not elevate cytosolic Ca or cAMP, although prolonged exposure to a Ca-free solution abolished the effect of MXS and 8) MXS-stimulated conductance was partially inhibited by diphenylamine-2-carboxylic acid, a blocker of Cl channels. The data suggest that MXS stimulates Cl channels, most likely depolarization-activated, outwardly rectifying channels. In contrast, the parent compound MX hyperpolarized the membrane potential and stimulated outward current without elevating cytosolic Ca and was independent of extracellular Ca, suggesting that MX stimulates Ca-insensitive K currents.

Animals↗
PubMed1993

Topical minoxidil therapy for androgenic alopecia in the Middle East. The Middle-Eastern Topical Minoxidil Study Group.

BACKGROUND: A 48-week open label trial was conducted in five Middle-Eastern countries (Lebanon, Egypt, Saudi Arabia, Jordan, and the United Arab Emirates) to determine the safety and efficacy of 2% minoxidil in the treatment of early androgenic alopecia and to compare the response with Western countries. METHODS: One hundred and ninety-five men aged between 19 and 47 years were enrolled. The duration of their baldness varied from 6 months to 10 years, and they all showed a type III vertex or type IV of the modified Hamilton scale. Baldness pattern, diameter of the balding area, hair counting within a 2.5 cm bald patch as well as investigator's and patient's evaluation were regularly noted. RESULTS: No significant changes were observed in vital signs or laboratory parameters. Of the 161 patients considered evaluable at 48 weeks, 80% showed moderate to dense growth. The mean increase in nonvellus hair at 12 months was 234. CONCLUSIONS: The age of the patient and the type of baldness rather than its duration affected the final outcome.

Administration, Cutaneous↗
PubMed2004

A randomized, placebo-controlled trial of 5% and 2% topical minoxidil solutions in the treatment of female pattern hair loss.

BACKGROUND: To pical minoxidil solution 2% stimulates new hair growth and helps stop the loss of hair in men with androgenetic alopecia and women with female pattern hair loss. Results can be variable, and historic experience suggests that higher concentrations of topical minoxidil may enhance efficacy. OBJECTIVE: The purpose of this 48-week, double-blind, placebo-controlled, randomized, multicenter trial was to compare the efficacy and safety of 5% topical minoxidil with 2% topical minoxidil and placebo in the treatment of female pattern hair loss. METHODS: A total of 381 women (18-49 years old) with female pattern hair loss applied 5% topical minoxidil solution (n = 153), 2% topical minoxidil solution (n = 154), or placebo (vehicle for 5% solution; n = 74) twice daily. Primary efficacy variables were change in nonvellus hair count at week 48, and patient and investigator assessments of change in hair growth/scalp coverage at week 48. RESULTS: After 48 weeks of therapy, 5% topical minoxidil was superior to placebo for each of the 3 primary efficacy measures. The 2% topical minoxidil group demonstrated superiority over placebo for hair count and investigator assessment of hair growth/scalp coverage at week 48; differences in patient assessment of hair growth at week 48 were not significantly different from placebo. The 5% topical minoxidil group demonstrated statistical superiority over the 2% topical minoxidil group in the patient assessment of treatment benefit at week 48. Both 5% and 2% topical minoxidil helped improve psychosocial perceptions of hair loss in women with female pattern hair loss. An increased occurrence of pruritus, local irritation, and hypertrichosis was observed with 5% topical minoxidil versus 2% topical minoxidil and placebo. CONCLUSION: In this 48-week study of 381 women with female pattern hair loss, 5% topical minoxidil was superior to placebo on each of the 3 primary efficacy end points: promoting hair growth as measured by change in nonvellus hair count and patient/investigator assessments of hair growth and scalp coverage. Application of 2% topical minoxidil was superior to placebo for assessments of nonvellus hair counts and investigator assessment of hair growth/scalp coverage at week 48; differences in patient assessment of hair growth at week 48 were not significantly different from placebo. At week 48, the 5% topical minoxidil group demonstrated statistical superiority over the 2% topical minoxidil group in the patient assessment of treatment benefit. Both concentrations of topical minoxidil were well tolerated by the women in this trial without evidence of systemic adverse effects. With the introduction of numerous herbal remedies for hair loss, of which most have not been tested in randomized, double-blind, placebo-controlled trials, it is important to describe well-controlled trials that demonstrate the efficacy and safety of topical drugs.

Administration, Topical↗
PubMed1990

Minoxidil sulfate is the active metabolite that stimulates hair follicles.

An important step in understanding minoxidil's mechanism of action on hair follicles was to determine the drug's active form. We used organ-cultured vibrissa follicles to test whether it is minoxidil or its sulfated metabolite, minoxidil sulfate, that stimulates hair growth. Follicles from neonatal mice were cultured with or without drugs and effects were assessed by measuring incorporation of radiolabeled cysteine in hair shafts of the treated follicles. Assays of minoxidil sulfotransferase activity indicated that vibrissae follicles metabolize minoxidil to minoxidil sulfate. Dose-response studies showed that minoxidil sulfate is 14 times more potent than minoxidil in stimulating cysteine incorporation in cultured follicles. Three drugs that block production of intrafollicular minoxidil sulfate were tested for their effects on drug-induced hair growth. Diethylcarbamazine proved to be a noncompetitive inhibitor of sulfotransferase and prevented hair growth stimulation by minoxidil but not by minoxidil sulfate. Inhibiting the formation of intracellular PAPS with chlorate also blocked the action of minoxidil but not of minoxidil sulfate. Acetaminophen, a potent sulfate scavenger blocked cysteine incorporation by minoxidil. It also blocked follicular stimulation by minoxidil sulfate apparently by directly removing the sulfate from the drug. Experiments with U-51,607, a potent minoxidil analog that also forms a sulfated metabolite, showed that its activity was inhibited by both chlorate and diethylcarbamazine. These studies show that sulfation is a critical step for hair-growth effects of minoxidil and that it is the sulfated metabolite that directly affects hair follicles.

Acetaminophen↗
PubMed2001

Effect of minoxidil on rabbit lens epithelial cell behavior in vitro and in situ.

BACKGROUND: Lens epithelial cell (LEC) proliferation and the associated production of extracellular matrix (ECM) are responsible for capsular opacification after cataract-IOL surgery. Minoxidil is an inhibitor of lysyl hydroxylase, an enzyme involved in procollagen hydroxylation. To evaluate the potential efficacy of minoxidil in inhibiting postoperative capsular opacification, we examined the effects of minoxidil on LEC behavior in cell and organ cultures. METHODS: We examined minoxidil effects on collagen production, migration and proliferation of cultured rabbit LECs as well as its ultrastructural effects, and also its effects on the cell population in organ-cultured capsular bag. RESULTS: No cytotoxicity was identified by MTT assay at the concentrations up to 3.0 mM of minoxidil, whereas it decreased the collagen production in LECs. Minoxidil also inhibited migration and proliferation of cells. Ultrastructural observation revealed the presence of dilated endoplasmic reticulum in LECs treated with minoxidil, indicating the accumulation of protein, probably underhydroxylated collagen precursors. The capsules cultured with minoxidil appeared less opaque than control specimens. On histological examination the numbers of cells on equatorial capsules were found to be significantly lower in minoxidil culture than in control culture. No lens cells were detected on the central posterior capsule of minoxidil culture, whereas they were seen in control. CONCLUSION: Minoxidil inhibited LEC migration and proliferation in vitro, as well as collagen secretion. Collagen secretion may be essential for LEC migration and proliferation. Minoxidil also attenuated repopulation of LECs on the inner surface of organ-cultured capsules. Minoxidil may be a potential inhibitor of postoperative capsular opacification.

Animals↗
PubMed1998

Sulfation of minoxidil by multiple human cytosolic sulfotransferases.

Minoxidil is an antihypertensive agent and hair growth promoter that is metabolized by sulfation to the active compound, minoxidil sulfate. Thermostable phenol sulfotransferase (TS PST or P-PST) was initially thought to catalyze the reaction, and the enzyme was designated minoxidil sulfotransferase (MNX-ST). Information about human ST activities toward minoxidil would be useful in developing the capacity to predict individual responses to minoxidil based on tissue levels of STs. Therefore, human STs were studied from platelet homogenates, partially purified platelets, scalp skin high speed supernatants and COS-1 cell cDNA expressed preparations using a radiochemical enzymatic assay with minoxidil as the substrate. Studies showed the presence of TS PST, TL (thermolabile) PST and MNX-ST activities in human scalp skin. Biochemical properties and correlation studies suggested that in addition to TS PST, the TL PST activity, another ST activity or both were involved in the reaction. Partially purified human platelet TL PST tested with minoxidil and dopamine showed identical thermal stabilities and similar responses to the inhibitors 2,6-dichloro-4-nitrophenol (DCNP) and NaCl. To characterize the activity of TL PST toward minoxidil, several biochemical properties of the enzyme expressed from a human liver cDNA clone were investigated. When assayed with minoxidil and dopamine, thermal stabilities of the expressed enzyme were identical and IC50 values for the inhibitors DCNP and NaCl were similar. It was also demonstrated that cDNA encoded human liver dehydroepiandrosterone sulfotransferase and estrogen sulfotransferase contributed to the sulfation of minoxidil. The results confirm that at least four human STs contribute to minoxidil sulfation. MNX-ST activity represents a combination of ST activities. The data indicate that multiple ST activities should be taken into account in attempts to predict the regulation of minoxidil sulfation and individual responses to minoxidil.

Animals↗
PubMed1998

The effect of minoxidil on keratocyte proliferation in cell culture.

PURPOSE: To determine if minoxidil inhibits keratocyte proliferation in a nontoxic manner. METHODS: Rabbit keratocytes were cultured in Eagle's minimum essential medium supplemented with fetal bovine serum. Minoxidil varying in concentration from 10(0) to 10(3) micrograms/ml was added to the culture medium and incubated for 7 days. The cultures were inspected for morphologic appearance and the cell number was determined at 1, 3 and 7 days after the addition of minoxidil. After 7 days of incubation, minoxidil was withdrawn from the cell culture medium and the cells were examined 3 and 7 days thereafter. In addition, a nonradioactive cytotoxic assay was performed to determine if toxicity is associated with the presence of minoxidil. RESULTS: Minoxidil inhibited keratocyte proliferation in a dose-dependent fashion. 29% of control growth was achieved when keratocytes were cultured for 7 days in 10(3) micrograms/ml, whereas 82% control growth was achieved when keratocytes were cultured in 10(2) micrograms/ml of minoxidil. Intermediate concentrations between 10(2) and 10(3) micrograms/ml produced a linear decline in cell counts in a dose-dependent fashion. The concentration of minoxidil required for 50% control growth at 7 days extrapolated from the dose-response curve was 600 micrograms/ml. Upon withdrawal of minoxidil, cell counts returned to baseline for concentrations of 10(2) micrograms/ml or less. Phase contrast microscopy revealed that the presence of minoxidil was associated with intercellular separation, enlargement of cell bodies and elongated processes. After the withdrawal of minoxidil, the cells in all media reassumed the morphological features of normal keratocytes which included a regular fusiform shape and extensive intercellular contact. The nonradioactive cytotoxic assay revealed the lack of cytotoxicity at all concentrations of minoxidil based on a lack of lactate dehydrogenase release. CONCLUSIONS: Minoxidil inhibits keratocyte proliferation by a nontoxic mechanism. It might be particularly useful for modulating corneal wound healing following excimer laser photorefractive keratectomy.

Animals↗
PubMed1990

Immunohistochemical and autoradiographic findings suggest that minoxidil is not localized in specific cells of vibrissa, pelage, or scalp follicles.

Immunohistochemistry with a minoxidil antibody suggested that minoxidil-immunoreactivity is associated with the root sheaths, laterally orientated differentiating matrix cells, and dividing epithelial cells of cultured vibrissa follicles of pigmented and albino neonatal mice. The dermal papilla and connective tissue sheath were devoid of minoxidil-immunoreactivity. To verify that minoxodil-immunoreactivity in the follicles was specific, immunostaining was conducted with dissected whisker pads, formalin-fixed "dead" follicles, and sections of spleen, liver and kidney (non-haired organs) cultured with minoxidil. Microscopic examination revealed minoxidil-immunoreactivity in all of these tissues. Follicles and whisker pads cultured with minoxidil, then washed for one h in media were devoid of minoxidil-immunoreactivity. These data suggest that minoxidil-immunoreactivity in cultured vibrissa follicles is probably non-specific. Sections of skin from C3H and CF1 mice which were topically dosed with minoxidil (in vivo) showed no minoxidil-immunoreactivity. Autoradiography demonstrated that tritiated minoxidil was bound in vivo and in vitro only to melanin granules in pigmented follicles of rodent and human tissue. This is probably non-specific binding since melanin is known to accumulate several chemically and pharmacologically unrelated drugs. It is reasonable to conclude that, under the conditions of these experiments, minoxidil is not specifically localized in any cells of whisker, pelage or, scalp follicles.

Animals↗
PubMed1987

Action of topical minoxidil in the bald stump-tailed macaque.

The effect of topical minoxidil (5% and 2% solutions) on hair regrowth was studied in the frontal bald scalp of 18 adolescent and adult stump-tailed macaques (Macaca arctoides). Gross observation of the hairiness and folliculogram analysis of the skin biopsy specimens have shown that minoxidil induces the enlargement of vellus follicles to the size of middle to terminal follicles (regrowth of hair effect), minoxidil maintains the terminal follicles in the prebald scalp of periadolescent animals (prevention of baldness effect), enlarged follicles regress after minoxidil is withdrawn, and hair follicular growth is once again stimulated when treatment with minoxidil is reinstituted. Hair regrowth was more prominent in the early stage of baldness among younger macaques than in baldness of longer duration in older animals. An in vitro study of 3H thymidine uptake revealed that the hair follicles in minoxidil-treated macaque skin showed significant enhancement of deoxyribonucleic acid synthesis in the follicular and perifollicular cells but not in the epidermal keratinocytes. Furthermore, the uptake of 3H minoxidil and its conversion to minoxidil sulfate (the active metabolite producing vasodilation) was relatively higher in the hair follicles than in the epidermis and dermis. Serum concentration of minoxidil was fairly constant 2, 4, 6, 15, and 24 hours after a single application (averaging 15 ng/ml with 5% minoxidil). Minoxidil's essential action in hair follicular growth may be as a potent vasodilator. However, a direct action on the hair follicle cannot be ruled out considering uptake and conversion of the drug to minoxidil sulfate within the hair follicle itself.

Administration, Topical↗
PubMed1987

Androgenetic alopecia: treatment results with topical minoxidil.

A double-blind 12-month trial was conducted to evaluate the safety and efficacy of topical minoxidil in patients with androgenetic alopecia. During the first 4 months of the study, patients applied a topical solution containing either 2% minoxidil, 3% minoxidil, or placebo to their scalps twice daily. At the end of the fourth month, patients taking placebo were crossed over to treatment with 3% minoxidil solution. Of 60 patients enrolled in the study, 43 were evaluable at month 12. Hairs were counted in a 1-inch target area and classified as vellus, indeterminate, and terminal; the latter two classifications were combined as nonvellus hairs for further statistical analysis. All three groups had significant increases in total, nonvellus, and terminal hair counts between baseline and month 4 and between month 4 and month 12. At month 4 the average total hair counts increased from a baseline mean of 158.2 to 270.2 in the 2% minoxidil group, from 156.6 to 287.0 in the 3% minoxidil group, and from 162.6 to 246.9 in the placebo group. At month 12 the means were 415.6, 448.5, and 471.1 in the 2% minoxidil, 3% minoxidil, and placebo-3% minoxidil crossover subjects, respectively. The increases from month 4 to month 12 were highly significant for each group (p = 0.0001). Average increases in nonvellus hair counts between months 4 and 12 were 216, 181, and 264 in the 2% minoxidil, 3% minoxidil, and placebo-to-3% minoxidil crossover groups, respectively, all highly significant differences from zero (p = 0.0001).(ABSTRACT TRUNCATED AT 250 WORDS)

Administration, Topical↗
PubMed1995

The effect of minoxidil analogues and metabolites on the contraction of collagen lattices by human skin fibroblasts.

Minoxidil, in addition to its effect on hypertension and hair growth, has been proposed as a potential antifibrotic agent. Minoxidil inhibits the contraction of collagen lattices by human fibroblasts in vitro. However, the mechanism of inhibition is unknown. As minoxidil is metabolised in the body to minoxidil glucuronide and minoxidil sulphate, we investigated the potencies of these metabolites to inhibit collagen lattice contraction. We also studied selected analogues of minoxidil to assess the influence of certain functional groups in the inhibition. The major metabolite, minoxidil glucuronide, proved to be inactive, whereas minoxidil sulphate was considerably more active than minoxidil. In terms of the structural analogues, the substitution of one amino group by a methyl group resulted in loss of the inhibitory activity; removal of the nitroxide oxygen led to stronger inhibition than with minoxidil. Further studies are planned to learn more about a possible role for minoxidil in wound contraction.

Animals↗
PubMed2004

Effect of minoxidil on proliferation and apoptosis in dermal papilla cells of human hair follicle.

BACKGROUND: Minoxidil has been widely used to treat androgenetic alopecia, but little is known about its pharmacological activity or about the identity of its target cells in hair follicles. We hypothesized that minoxidil has direct effects on the proliferation and apoptosis of dermal papilla cells (DPCs) of human hair follicle. OBJECTIVE: To elucidate the mechanism of topical minoxidil action in terms of stimulating hair growth. METHODS: We evaluated cell proliferations in cultured DPCs by 3-(4,5-dimethylthiazol-2-yl)-2,5-diphenyl tetrazolium bromide (MTT) and measured the expressions of extracellular signal-regulated kinase (ERK), Akt, Bcl-2, and Bax by Western blot. We also measured elongation of hair follicles in organ culture. RESULTS: Minoxidil significantly increased the proliferation of DPCs. The levels of ERK phosphorylation and of phosphorylated Akt increased significantly 1 h post-treatment; percentage increase of ERK phosphorylation was 287% at 0.1 microM and 351% at 1.0 microM of minoxidil, and that of Akt phosphorylation was 168% at 0.1 microM and 257% at 1.0 microM of minoxidil. 1.0 microM of minoxidil increased Bcl-2 expression over 150%, while 1.0 microM of minoxidil decreased Bax expression by more than 50%. Moreover, a significant elongation of individual hair follicles in organ culture was observed after adding minoxidil. CONCLUSION: Minoxidil promotes the survival of human DPCs by activating both ERK and Akt and by preventing cell death by increasing the ratio of Bcl-2/Bax. We suggest that minoxidil stimulates the growth of human hairs by prolonging anagen through these proliferative and anti-apoptotic effects on DPCs.

Adult↗