Ac-SKDP is a pro-angiogenic peptide degradation product of thymosin B4 that regulates hematopoiesis by inhibiting proliferation of hematopoietic pluripotent stem cells (spleen colony-forming units, or CFUs). This peptide exhibits cardioprotective, anti-inflammatory, and anti-fibrotic activities. In animal models of chronic myocardial infarction, Ac-SDKP improves left ventricular function, increases angiogenesis, and decreases infarct size. In hypertensive rats, Ac-SDKP prevents angiotensin II-induced increases in collagen synthesis and cross-linking as well as expression of LOX and TGF-β and activation of NF-κB and lymphocytic immune cells. In other animal models, this peptide prevents fibrosis, decreasing deposition of fibronectin and collagen and decreasing the number of myofibroblasts and macrophages. Ac-SDKP also exhibits nephroprotective activity, inhibiting progression of lupus nephritis in animal models; Ac-SDKP decreases proteinuria, infiltration of inflammatory T cells and macrophages, production of TNF-α, activation of NF-κB, and phosphorylation of Smad2/3, resulting in improvements in renal function.