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1 and 4.4 events per patient-year with insulin lispro.
2 or glargine U100, both with prandial insulin lispro.
3 ec (n=349), both in combination with insulin lispro.
4 te of hypoglycemia was 12% less with insulin lispro (6.4 +/- 0.2 vs. 7.2 +/- 0.3 episodes/30 days, P
8 ve types of insulin (human, bovine, porcine, Lispro, and Lantus) were used as model products in the s
9 tudies employed Lys(B28), Pro(B29)-insulin ("lispro") as a model prandial analog that is less thermod
10 ty of tirzepatide (pooled cohort) vs insulin lispro, both in addition to insulin glargine, in HbA1c c
11 ucose; for instance, the fast-acting insulin lispro contains two point mutations that suppress dimer
13 kg with tirzepatide and 3.2 kg with insulin lispro (estimated treatment difference, -12.2 kg [95% CI
14 s regular, neutral protamine Hagedorn [NPH], lispro, glulisine, glargine, detemir, degludec, and aspa
15 ir and sofosbuvir tablets [Harvoni], insulin lispro [Humalog], and insulin aspart [Novolog]) and thei
18 tiated, including human insulin (P28K29) and Lispro insulin (K28P29), which differ only by the interc
19 ed as prandial insulin (for example, insulin lispro, insulin aspart, or insulin glulisine) and basal
25 glargine once daily and rapid-acting insulin lispro or aspart before meals (the basal-bolus group) du
27 eas treatment with insulin aspart or insulin lispro or to receive standard care (defined as any insul
30 oled cohort) was -2.1% vs -1.1% with insulin lispro, resulting in mean HbA1c levels of 6.7% vs 7.7% (
31 f insulin-specific antibodies (ISA), insulin lispro-specific antibodies (LSA), and cross-reactive ant
33 hypoglycemic episodes was less with insulin lispro than with regular human insulin therapy during th
35 ting this allosteric switch, 3-iodo-Tyr(B26)-lispro thus illustrates how a nonstandard amino acid sub
36 t tyrosine adjoining the engineered sites in lispro (Tyr(B26)) by 3-iodo-Tyr (i) augments its thermod
38 we contrasted the immunogenicity of insulin lispro versus regular human insulin (RHI) in patients pr