Seven transmembrane G protein-coupled receptors (GPCRs) have gained much interest in recent years as it is the largest class among cell surface receptors. G proteins lie in the heart of GPCRs signalling and therefore can be therapeutically targeted to overcome complexities in GPCR responses and signalling. G proteins are classified into four families (G(i), G(s), G(12/13) and G(q)); G(q) is further subdivided into four classes. Among them G(alpha q) and G(alpha q/11) isoforms are most crucial and ubiquitously expressed; these isoforms are almost 88% similar at their amino acid sequence but may exhibit functional divergences. However, uncertainties often arise about G(alpha q) and G(alpha q/11) inhibitors, these G proteins might also have suitability to the invention of novel-specific inhibitors for each isoforms. YM-254890 and UBO-QIC are discovered as potent inhibitors of G(alpha q) functions and also investigated in thrombin protease-activated receptor (PAR)-1 inhibitors and platelet aggregation inhibition. The most likely G protein involved in PAR-1 stimulates responses is one of the G(alpha q) family isoforms. In this review, we highlight the molecular structures and pharmacological responses of G(alpha q) family which may reflect the biochemical and molecular role of G(alpha q) and G(alpha q/11). The advanced understanding of G(alpha q) and G(alpha q/11) role in GPCR signalling may shed light on our understanding on cell biology, cellular physiology and pathophysiology and also lead to the development of novel therapeutic agents for a number of diseases.