Peroxisome proliferator-activated receptor (PPAR) $gamma$ is known to be a key regulator of insulin resistance. PAR-1622 is a novel small molecule compound synthesized in Dong-A research center. In this study, we characterized the pharmacological profiles of PAR-1622, a selective partial activator of $PPAR{gamma}$. In transient transactivation assays, PAR-1622 [(S)-2-ethoxy-3(4-(5-(4-(5-(methoxymethyl)isoxazol-3-yl)phenyl)-3-methylthiophen-2-yl)methoxy)phenyl)propanoic acid] showed a partial activator against human $PPAR{gamma}$ with an $EC_{50}$ of 41 nM and a maximal response of 37% relative to the full agonist rosiglitazone without activating human $PPAR{delta}$. PAR-1622 was 56 folds more selective for human $PPAR{gamma}$ than for human $PPAR{alpha}$ ($EC_{50}$, 2304 nM), which means that it is a selective partial activator of $PPAR{gamma}$. PAR-1622 also showed a partial activator against mouse $PPAR{gamma}$ with an $EC_{50}$ of 427 nM and a maximal response was 57% of that of rosiglitazone. INT-131, a selective $PPAR{gamma}$ partial agonist in clinical stage, also was a partial activator against human $PPAR{gamma}$ with an $EC_{50}$ of 83 nM and a maximal response achieved by INT-131 was 49% of that observed with full agonist rosiglitazone. In functional assays using human mesenchymal stem cells, PAR-1622 induced adipocyte differentiation, which was 3-fold more potent with a comparable maximum response compared to INT-131. Furthermore, PAR-1622 significantly improved hyperglycemia in db/db when orally administered at a dose of 1 mg/kg/day for 5 days. In hemodilution assays with Evans Blue, rosiglitazone significantly increased the plasma volume in ICR mice that were orally administered 30 mg/kg/day for 9 days; however, PAR-1622 showed no significant effects on plasma volume, similar to INT-131. These results suggest that PAR-1622 is a selective partial activator of $PPAR{gamma}$ and has excellent antihyperglycemic activities and a broad safety profile for fluid retention.