ErgoNex Pharma has licensed the development rights on Terguride. Oral formulations of terguride have been approved in the treatment of hyperprolactinemic pituitary adenoma, ovulation disorders due to hyperprolactinemia, galactorrhea and suppression of puerperal lactation. Terguride has a benign side effect profile, which is well established in clinical use and confirmed by post-marketing surveillance studies.

ErgoNex Pharma is presently studying the clinical utilities of Terguride in FMS and PAH in clinical proof-of-concept studies.

Terguride modulates a spectrum of neurotransmitter receptors including dopamine, serotonin, and alpha2-adrenergic receptors with high affinity.

Terguride has the unique potential to influence unbalanced dopaminergic systems, by acting as an agonist under conditions of short supply, while inhibiting receptor activation under conditions of excess stimulation. Suppression of prolactin (PRL) is indicative of dopamine agonist action on the hypophyseal dopamine system. Dopamine agonistic effects of Terguride were also evident in rats with unilateral nigral 6-hydroxy-dopamine lesions (i.e. a model of Parkinson´s disease). Disturbances of normal dopaminergic function have also been implicated in FMS. Dopamine controls the subjective rating of pain severity, the anticipation and emotional response to pain as well as adaptive stress response. In the presence of a relative dopaminergic deficit pain signals reach the brain unfiltered and contribute to chronic pain states. Alterations in dopaminergic neurotransmission and of structural changes in brains of FMS patients have been demonstrated by PET and fMRI imaging. Terguride acts as dopaminergic agonist and corrects this deficit.

Terguride is a strong anti-serotoninergic drug and acts as an antagonist of the 5-HT2 receptors. 5-HT2 receptor isoforms have been implicated in trophic effects of serotonin (5-HT). Excessive vascular remodeling processes or fibrosis, respectively, in a number of tissues including liver, kidney, heart valve and lung have been associated with altered 5-HT signalling or metabolism. In pulmonary arterial hypertension (PAH) and idiopathic pulmonary fibrosis (IPF) 5-HT has been implicated in excessive wound healing processes with extensive proliferation of arterial smooth muscle cells in PAH, or transformation of fibroblasts into an extracellular matrix depositing fibromyoblast phenotype in lung parenchyma. In pulmonary hypertension 5-HT receptor signalling plays a key role in pulmonary vascular remodelling processes, which are the main driving force for the advanced stages of the disease. Excessive proliferative effects of 5-HT also manifest in cardiomyocytes and contribute directly to progression to heart failure. Terguride has potent anti-proliferative and anti-fibrotic activity and thereby drives reverse remodelling processes.