1 g/kg to a high of 2.9 g/kg. For comparison, the lower doses in study C97-1243 overlapped with doses
of P188-NF that yielded unacceptable renal toxicity in AMI patients, while the higher doses exceeded the maximum doses of P188-NF by almost 2-fold. Study C97-1243 also included renal function studies to assess the effect of P188-P on the nephron. These assessments were performed on specimens collected at baseline and upon completion of the P188-P infusion, as well as on specimens collected 1 day, 2 days, 3 days, 5–10 days, and 28–35 days after the infusion. The tests that were utilized, and the renal functions they evaluate (as indicated in parentheses) PF-6463922 nmr are as follows: serum creatinine (glomerular filtration), creatinine clearance (glomerular filtration), β-N-acetylglucosaminidase levels (tubular injury), retinol binding protein levels (protein absorption pathways), albumin (integrity of glomerulus), immunoglobulin G (IgG) excretion
(glomerulus permeability), and urine osmolarity (distal tubular transport). Figure 6 presents the mean serum creatinine levels in the dose groups in study C97-1243 during and after a 24-h intravenous infusion of P188-P. The mean baseline creatinine levels were within normal ranges for all dose groups (<136 μmol/L [<1.5 mg/dL] in men and <120 μmol/L [<1.4 mg/dL] in women) . Following treatment, the mean values generally remained within the normal range and there were mTOR inhibitor no clear dose-related else changes. In one group (receiving 100 mg/kg/h), the data were skewed by a single subject who developed septic shock with kidney failure, which
was determined by the investigator to be unrelated to the treatment. Similarly, a transient rise in serum creatinine on day 2 was observed in the 120 mg/kg/h group. This also was unlikely to be indicative of a treatment-related effect, since it was driven by a value from a single individual whose baseline value was 1.2 mg/dL and where the day 2 value actually represented a decrease from baseline. Excluding these outliers, the data support that treatment with P188-P does not result in differences in mean serum creatinine across the dose range studied. Fig. 6 Serum creatinine levels in JSH-23 solubility dmso patients treated with purified poloxamer 188 (P188-P). Each bar represents the mean ± standard deviation for measurements conducted in the indicated group Figure 7 presents mean creatinine clearance values for the dose groups in study C97-1243 during and after a 24-h intravenous infusion of P188-P. Consistent with the serum creatinine results, the serum creatinine clearance data does not identify any dose-related changes or clinically significant effects across time. A transient change in creatinine clearance at day 2 was observed in the 120 mg/kg/h group; however, this likely was influenced by the results from a single subject, as previously noted. Fig. 7 Serum creatinine clearance in patients treated with purified poloxamer 188 (P188-P).