Bio-Behavioral Changes Following Transition to Automated Insulin Delivery: A Large Real-Life Database Analysis

   Objective: Document glycemic and user-initiated bolus changes following transition from predictive-low glucose suspend (PLGS) system to automated insulin delivery (AID) system during real-life use. Research Design and Methods: Analysis of 2,329,166 days (6,381 patient-years) of continuous glucose monitoring (CGM) and insulin therapy data for 19,354 individuals with Type 1 Diabetes, during 1-month PLGS (Basal-IQ technology) use followed by 3-month AID use (Control-IQ technology). Baseline characteristics: 55.4 percent female, age (median/quartiles/range) 39/19-58/1-92 years, glucose management indicator (GMI) 7.5±0.8. Primary outcome: time in target range (TIR 70-180mg/dL). Secondary outcomes: CGM-based glycemic control metrics; frequency of user-initiated boluses. Results: Compared to PLGS, AID increased TIR on average from 58.4 to 70.5 percent. GMI and percent time above/below target range improved as well, 7.5 to 7.1; 39.9 to 28.1 percent, and 1.66 to 1.46 percent, respectively, all p-levels 8.0 (TIR improvement 13.2 percentage points). User-initiated correction boluses decreased from 2.7 to 1.8 per day, while user-initiated meal boluses remained stable at 3.6 to 3.8 per day. Conclusions: Observed in real life of over 19,000 individuals with type 1 diabetes, transitions from PLGS to AID resulted in improvement of all glycemic parameters, equivalent to improvements observed in randomized clinical trials, and reduced user-initiated boluses.  However, glycemic and behavioral changes with AID use may differ greatly across different demographic and clinical groups. </p

sj-docx-1-dst-10.1177_19322968241229074 – Supplemental material for Safety and Feasibility Evaluation of Automated User Profile Settings Initialization and Adaptation With Control-IQ Technology

Supplemental material, sj-docx-1-dst-10.1177_19322968241229074 for Safety and Feasibility Evaluation of Automated User Profile Settings Initialization and Adaptation With Control-IQ Technology by Viral N. Shah, Halis K. Akturk, Alex Trahan, Nicole Piquette, Alex Wheatcroft, Elain Schertz, Karen Carmello, Lars Mueller, Kirstin White, Larry Fu, Ravid Sassan-Katchalski, Laurel H. Messer, Steph Habif, Alex Constantin and Jordan E. Pinsker in Journal of Diabetes Science and Technology</p

sj-docx-3-dst-10.1177_19322968241229074 – Supplemental material for Safety and Feasibility Evaluation of Automated User Profile Settings Initialization and Adaptation With Control-IQ Technology

Supplemental material, sj-docx-3-dst-10.1177_19322968241229074 for Safety and Feasibility Evaluation of Automated User Profile Settings Initialization and Adaptation With Control-IQ Technology by Viral N. Shah, Halis K. Akturk, Alex Trahan, Nicole Piquette, Alex Wheatcroft, Elain Schertz, Karen Carmello, Lars Mueller, Kirstin White, Larry Fu, Ravid Sassan-Katchalski, Laurel H. Messer, Steph Habif, Alex Constantin and Jordan E. Pinsker in Journal of Diabetes Science and Technology</p

sj-docx-2-dst-10.1177_19322968241229074 – Supplemental material for Safety and Feasibility Evaluation of Automated User Profile Settings Initialization and Adaptation With Control-IQ Technology

Supplemental material, sj-docx-2-dst-10.1177_19322968241229074 for Safety and Feasibility Evaluation of Automated User Profile Settings Initialization and Adaptation With Control-IQ Technology by Viral N. Shah, Halis K. Akturk, Alex Trahan, Nicole Piquette, Alex Wheatcroft, Elain Schertz, Karen Carmello, Lars Mueller, Kirstin White, Larry Fu, Ravid Sassan-Katchalski, Laurel H. Messer, Steph Habif, Alex Constantin and Jordan E. Pinsker in Journal of Diabetes Science and Technology</p

Discovery of (<i>S</i>)‑1-(1-(4-Chloro-3-fluorophenyl)-2-hydroxyethyl)-4-(2-((1-methyl‑1<i>H</i>‑pyrazol-5-yl)amino)pyrimidin-4-yl)pyridin-2(1<i>H</i>)‑one (GDC-0994), an Extracellular Signal-Regulated Kinase 1/2 (ERK1/2) Inhibitor in Early Clinical Development

The extracellular signal-regulated kinases ERK1/2 represent an essential node within the RAS/RAF/MEK/ERK signaling cascade that is commonly activated by oncogenic mutations in BRAF or RAS or by upstream oncogenic signaling. While targeting upstream nodes with RAF and MEK inhibitors has proven effective clinically, resistance frequently develops through reactivation of the pathway. Simultaneous targeting of multiple nodes in the pathway, such as MEK and ERK, offers the prospect of enhanced efficacy as well as reduced potential for acquired resistance. Described herein is the discovery and characterization of GDC-0994 (<b>22</b>), an orally bioavailable small molecule inhibitor selective for ERK kinase activity