for educational and safety purposes
Every compound in the sci-wiki that affects insulin; the ones you can source are floated to the front, then the reference-only entries. Tap any for the full entry, mechanism, and outlets.
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ATR-258 is an investigational, GRK2-biased beta2 adrenergic receptor agonist developed by the Swedish company Atrogi AB for type 2 diabetes and obesity [2]. It emerged from a 2025 Cell paper in which ligand-based virtual screening and chemical evolution produced GRK-biased adrenergic agonists, with compound 15 shown to drive insulin-independent glucose uptake while avoiding the Gs and beta-arrestin signaling that limit classical beta2 agonists [1]. The rationale rests on a decade of GRK2 biology: GRK2 upregulation and Gi-biased beta2AR signaling are linked to heart failure and metabolic dysregulation [5], and GRK2-biased transduction is now framed as a distinct therapeutic axis beyond G protein and arrestin signaling [3]. A 2026 perspective argues the biased agonist paradigm for diabetes and obesity is edging toward clinical reality [4]. Mechanism-context studies on GRK2 in beta-adrenergic signaling and blood pressure regulation support the class biology [6] [7]. Atrogi has advanced follow-on candidates into early human testing per company announcements, but no clinical results are published; the evidence base is preclinical.
INT131 (also written INT-131, formerly T131 and AMG131) is an experimental oral drug for type 2 diabetes, developed by InteKrin Therapeutics as a selective PPAR-gamma modulator (SPPARM). Unlike the older thiazolidinedione insulin sensitizers, it only partially activates the PPAR-gamma receptor, a design intended to keep the blood-sugar benefits of that drug class while avoiding side effects such as weight gain and fluid retention. It reached mid-stage clinical trials but is not an approved medicine.