The α1A- and α1B- adrenoceptors (α1A-AR & α1B-AR) are clinically important G protein-coupled receptors (GPCRs) classically known for their physiological function of regulating smooth muscle contractility and blood pressure. They are targeted by non-selective α1-blockers for the treatment of hypertension and benign prostatic hyperplasia. These receptors are also highly expressed in the CNS and the myocardium and recently it has become clear that selective stimulation of the α1A-AR subtype might lead to beneficial outcomes in patients with heart failure and provide neuroprotection in neurodegenerative disease. On the other hand, some studies suggest that chronic signaling by α1B-AR is cardiac damaging, neurodegenerative and pro-apoptotic. Therefore, selective targeting of these receptors with α1A-AR agonists and & α1B-AR antagonist may be of importance for cardioprotection during heart failure and for neuroprotection in neurodegenerative disease. However, a detailed understanding of the individual roles of α1A-AR & α1B-ARs remains lacking and selective ligands are required to further understand their specific roles. We have engineered stabilised variants of human α1A-AR and α1B-AR for structural biology and recently used these purified proteins in an NMR- and SPR-based fragment screen. This trial fragment screen identified two structurally distinct fragments with unique receptor subtype selective properties. The first fragment (Cpd 1) displays 10-fold selectivity for inhibiting α1B-AR over α1A-AR. This represents an ideal starting point for developing a much needed α1B-AR-selective antagonist. The second fragment (Cpd 2), exhibits a dual functional profile, being a partial α1A-AR agonist and a relatively potent α1B-AR antagonist. Preliminary data also suggest an allosteric binding mode of Cpd 2. To date, we have screened several structural analogues of both compounds to increase our understanding of how these compounds bind and inform future medicinal chemistry. These newly identified ligands provide new pharmacological tools and may lead to more selective therapeutic agents for these clinically important GPCRs.