Neurokinin B

Reproductive / Menopause

Also known as: NKB, Neuromedin K, Neurokinin-B, TAC3

TachykininsResearch phase: Endogenous peptide (drug target for menopause)Regulatory: Endogenous peptide. NK3R antagonist fezolinetant (Veozah) is FDA-approved for menopausal vasomotor symptoms.

Mechanism

Neurokinin B is the tachykinin peptide most important for reproduction. It is part of the KNDy neuron system (Kisspeptin/NKB/Dynorphin) that controls GnRH pulsatility. NKB drives GnRH pulses while dynorphin terminates them. This discovery led directly to the development of NK3 receptor antagonists (like fezolinetant/Veozah) for treating menopausal hot flashes, which are caused by dysfunctional NKB signaling.

Technical detail

Neurokinin B (Asp-Met-His-Asp-Phe-Phe-Val-Gly-Leu-Met-NH2) is a 10-amino-acid tachykinin encoded by the TAC3 gene. It preferentially activates NK3R (TACR3, Gq-coupled) on KNDy neurons in the arcuate nucleus. NKB-NK3R signaling stimulates kisspeptin release, which drives pulsatile GnRH secretion. Loss-of-function mutations in TAC3 or TACR3 cause hypogonadotropic hypogonadism. During menopause, estrogen withdrawal disinhibits NKB signaling, driving thermoregulatory dysfunction (hot flashes) via projections to the preoptic area. NK3R antagonists (fezolinetant, pavinetant) reduce hot flash frequency by 50-75% without hormone replacement.

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