N,N-dimethylglycine sodium salt prevents human dermal papilla senescence and promotes hair growth in patients with pattern hair loss.

BACKGROUND

In our previous studies, N,N-dimethylglycine sodium salt (DMG-Na) was found to exert anti-inflammatory and anti-oxidant effects in human epidermal keratinocytes and promote the synthesis of regenerating growth factors (e.g., vascular endothelial growth factor).

OBJECTIVE

In the current investigation, we assessed the effects of DMG-Na to modulate hair follicle-derived dermal papilla (DP) senescence induced by oxidative (H2O2) or non-oxidative (Bromodeoxyuridine) stimuli using in vitro cultured human DP cells. Further, in two randomized, double-blind, placebo-controlled, parallel-group, sex-stratified in vivo studies, we determined the efficacy of a topical DMG-Na containing formulation on more than three hundred patients with hair loss.

METHODS

In the in vitro arm, intracellular Ca2+ measurements, senescence-associated β-galactosidase determinations, qRT-PCR assays, and various immunolabeling methods were employed whereas multiple hair loss parameters were assessed in the in vivo human studies.

RESULTS

DMG-Na (0.05%) significantly prevented the effects of H2O2 and Bromodeoxyuridine to upregulate the number of SA-β-Gal positive cells. Likewise, DMG-Na significantly normalized the expressions of several upregulated (e.g., matrix metalloproteinases 1 and 3, p21, interleukin-1β, tumor necrosis factor-α) or downregulated (e.g., Ki67, lamin B1, collagens 1A1 and 3A1) senescence-associated markers by the inducers. In line with these anti-senescence effects, in the human trials, topical formulations containing 0.5% DMG-Na significantly improved hair loss parameters.

CONCLUSION

Our findings - together with our prior evidence that topically applied DMG-Na enhanced skin blood flow in humans - collectively suggest that DMG-Na is an effective and promising active for the management of hair conditions characterized by impaired cellular growth, repair, and dysregulated oxidative metabolic status.