GTS 21 dihydrochloride is a novel agonist of nicotinic acetylcholine receptors (nAChRs) [1].
nAChRs are neuron receptor proteins that activated by the binding of the neurotransmitter acetylcholine (ACh).  
In RAW 264.7 cells (a macrophage like cell line) exposed to hyperoxia (≥99% O2), GTS-21 significantly increased phagocytic activity of macrophages in a dose-dependent way and reduced hyperoxia-induced hyperacetylation of HMGB1. Also, GTS-21 inhibited the cytoplasmic translocation and release of HMGB1 from these macrophages [1]. GTS-21 bound to human α4β2 nAChR (Ki value of 20 nM) 100-fold more potently than to human α7 nAChR, and was 2- and 18-fold less potent than (2)-nicotine at human α7 and α4β2 nAChR, respectively [2].    
In mice that were exposed to hyperoxia (≥99% O2) and subsequently challenged with PA, intraperitoneal injection of GTS-21 (4 mg/kg) significantly increased bacterial clearance, decreased accumulation of airway HMGB1 and decreased acute lung injury [1]. GTS-21 stimulated dopamine release from rat striatal slices with an EC50 of 10uM. In the delayed matching-to-sample task, GTS-21 (32–130 nmol/kg) improved learning performance of monkeys [2].
References:
[1]. Sitapara RA, Antoine DJ, Sharma L, et al. The α7 nicotinic acetylcholine receptor agonist GTS-21 improves bacterial clearance in mice by restoring hyperoxia-compromised macrophage function. Mol Med, 2014, 20: 238-247.
[2]. Briggs CA, Anderson DJ, Brioni JD, et al. Functional characterization of the novel neuronal nicotinic acetylcholine receptor ligand GTS-21 in vitro and in vivo. Pharmacol Biochem Behav, 1997, 57(1-2): 231-241.