Umbilical cord blood derived mesenchymal stem cells (UCB-MSCs) are emerging as a promising source for cell-based therapies especially allogenic transplantation. Each UCB-MSC has a different genetic background, although they all fall within the UCB-MSCs standard. There are no reports, however, on individual variations in the therapeutic efficacy of UCB-MSCs. For allogenic therapy, efficacy variation is may be a bottleneck for standardization of therapeutic protocols. In this study, to observe the existence of the individual variation in therapeutic efficacies, we established and characterized 4 UCB-MSCs from 4 different donors according to standard operating procedures. By FACS analysis we determined the phenotype of UCB-derived cells. All of UCB-derived cells expressed human MSC-specific immunophenotypes: they were positive for CD29, CD44, CD73, CD105, CD166, and HLA-ABC and negative for CD34, CD45 and HLA-DR. In addition, all these cells exhibited immunosuppressive ability in the mixed lymphocyte reaction (MLR) test. All the cells showed similar proliferation potency. The cells mainly had a bipolar fibroblast-like morphology, and all the cells had the potency for differentiation into multiple lineages. We named the 4 types of UCB-derived cells as M01, M02, M03, and M04. To investigate whether UCB-MSCs from different donors have varying therapeutic efficacy, we used post-infarction left ventricular (LV) remodeling in rat myocardial infarct (MI) model. Eight weeks after cell transplantation, LV remodeling was evaluated by echocardiography and by analyzing histological data. Interestingly, among the 4 UCB-MSCs, M02 showed the most efficacies in improving the LV systolic function, reducing the LV end-systolic dimension, reducing the infarct area, and preserving the wall thickness. In vivo data showed the existence of variations in therapeutic efficacy among UCB-MSCs. To determine the signature of individual variations in the UCB-MSCs, we performed DNA microarray analysis by using M02 and M01 cells that showed the best and worst efficacy, respectively, in MI repair in rats, and selected the cell surface-related genes that had a high expression level in M02 cells. We detected X-factor expression among M01, M02, M03, and M04, and obtained the coincident pattern with variation in in vivo efficacy. To detect X-factor function in UCB-MSCs, neutralization and overexpression were used, and we found that X-factor regulates the ERK-VEGF axis. Moreover, we obtained an interruption of tube formation by a VEGF-blocking conditioned supernatant of the UCB-MSC and in the peri-infarct area, the X-factor in the UCB-MSCs was found in the vessel structure that was located nearby and was detected by isolectin B4.