Introduction: Glucocorticoid-induced osteoporosis is an underrecognized complication of chronic glucocorticoid therapy characterized by a decrease in new bone formation. Anabolic therapies, such as teriparatide, a recombinant human parathyroid hormone, combat the disease by promoting new bone growth. Aims: This article outlines the pathophysiology of glucocorticoid-induced osteoporosis and details the evidence of efficacy, safety, and patterns of use of teriparatide and other future anabolic therapies. Evidence review: In multiple clinical trials, teriparatide has been shown to significantly increase lumbar spine bone mineral density (BMD) in patients with glucocorticoid-induced osteoporosis when compared with placebo, alendronate, and risedronate. When compared with alendronate, significantly fewer vertebral fractures were noted in the teriparatide group. Adverse effects noted in clinical trials include nausea, insomnia, flushing, myalgias, and mild hypercalcemia/hyperuricemia. Early studies in rats noted an increased incidence of osteosarcoma; however, an increased rate beyond levels seen in general populations has not been noted in human studies or with long-term pharmacovigilance. Abaloparatide and romosozumab are newer anabolic therapies that have shown some benefit in postmenopausal osteoporosis but have not yet been studied in the chronic glucocorticoid population. Place in therapy: Major specialty organizations continue to recommend bisphosphonates as first-line therapy in glucocorticoid-induced osteoporosis due to the proven benefit and relative affordability. However, the use of anabolics shows promise to improve outcomes by increasing BMD and reducing fracture-associated morbidity and mortality and has a role for selected populations at high fracture risk.