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Azoth Cards&Render_DUAL REGULATOR DIA-39-C20 10MG 3ML
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Dual Regulator DIA-39-C20

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Dual Regulator DIA-39-C20

HPLC Certified

CAS #:

2023788-19-2

Formula:

C225H348N48O68

M.W.:

4813.53

PURITY

≥99%

RUO

(Research use only)

SKU: AZ-DIA39C20-10 / AZ-DIA39C20-20 / AZ-DIA39C20-30

Specs: Amount: 10mg / 20mg / 30mg | Format: Lyophilized Powder | Container: 3mL Vial | Storage: 2-8°C | Type: Regulator Peptide / Peptide Research Compound | Research Category: Peptide Receptor Pathway Research

Azoth Cards&Render_DUAL REGULATOR DIA-39-C20 10MG 3ML

Dual Regulator DIA-39-C20

  • Fulfillment Timing Based on Inventory and Account Status

REV

Dual Regulator DIA-39-C20

CAS #:

2023788-19-2

Formula:

C225H348N48O68

M.W.:

4813.53

PURITY

≥99%

RUO

Research use only

Specs: Amount: 10mg / 20mg / 30mg | Format: Lyophilized Powder | Container: 3mL Vial | Storage: 2-8°C | Type: Regulator Peptide / Peptide Research Compound | Research Category: Peptide Receptor Pathway Research

What Is Dual Regulator DIA-39-C20?

Dual Regulator DIA-39-C20 is a synthetic 39-amino acid acylated peptide engineered from a GIP peptide backbone, designed for research into simultaneous activation of two distinct incretin receptor pathways: the glucose-dependent insulinotropic polypeptide receptor (GIPR) and the glucagon-like peptide-1 receptor (GLP-1R). With a molecular formula of C225H348N48O68 and a molecular weight of 4813.45 g/mol (CAS 2023788-19-2), this compound occupies a structurally distinct position from single-target GLP-1R agonists, incorporating modifications at key residues to enable balanced engagement of both receptor systems from a single molecular entity. Its structure is based on the GIP sequence and includes a C20 fatty diacid moiety that prolongs the duration of action through albumin binding, making it a relevant reference compound for researchers studying extended-half-life peptide pharmacokinetics alongside multi-receptor signaling. At Azoth, we offer Dual Regulator DIA-39-C20 synthesized to ≥99% purity, intended exclusively for licensed researchers and laboratory professionals.

How Does Dual Regulator DIA-39-C20 Work? Two Receptor Pathways Explored

Dual Regulator DIA-39-C20 is studied for an imbalanced and biased dual receptor profile, engaging the GIP receptor with greater occupancy than the GLP-1 receptor at equivalent concentrations. This receptor selectivity pattern makes it a useful tool for researchers seeking to isolate the relative contributions of each pathway in in vitro and animal model systems.

GIP Receptor Signaling

Receptor binding at the GIPR increases intracellular cyclic adenosine monophosphate (cAMP) in pancreatic beta cells, stimulating glucose-dependent insulin secretion. GIPR is widely expressed in islets, gut, adipose tissue, and brain, and GIP stimulates lipolysis and inhibits insulin-induced lipogenesis in adipocyte models. Researchers studying adipocyte nutrient metabolism have used this compound class as a tool for investigating how GIPR agonism modulates fat tissue function independently of GLP-1R signaling.

GLP-1 Receptor Signaling

Signaling studies demonstrate that this compound class shows bias at the GLP-1 receptor to favor cAMP generation over beta-arrestin recruitment, coincident with a weaker ability to drive GLP-1 receptor internalization compared with native GLP-1. GLP-1 receptors are distributed across the endocrine pancreas, heart, stomach, adipose tissue, vagus nerve, and various regions of the central nervous system, and animal studies have shown that GLP-1 promotes beta cell neogenesis and proliferation while inhibiting apoptosis.

Biased Agonism and Receptor Crosstalk

Experiments in primary pancreatic islets reveal that beta-arrestin1 limits the insulin response to GLP-1 but not to GIP or this dual agonist class, suggesting that the biased agonism profile may enhance insulin secretion in preclinical models. The imbalanced receptor engagement — greater GIP receptor occupancy combined with biased GLP-1 receptor signaling — creates a pharmacological profile distinct from selective GLP-1R agonists, offering researchers a model system for studying how these two pathways interact when co-activated simultaneously.

Adipose Tissue as a Direct Mechanistic Target

Adipose tissue is a potential direct mechanistic target of dual GIPR and GLP-1R agonists in contrast to GLP-1R monoagonists, since GIPR but not GLP-1R is expressed in adipose tissue. Preclinical and in vitro studies confirm the ability of GIPR/GLP-1R agonists to directly regulate adipose tissue function, illustrating modulation of adipocyte function as an important mechanistic target of this compound class. 

Buy Dual Regulator DIA-39-C20 for These Research Applications

Dual Incretin Receptor Pharmacology

The primary research interest in this compound class centers on dissecting the respective contributions of GIP and GLP-1 receptor activation when engaged simultaneously by a single molecule rather than separate compounds. Available preclinical data indicate that dual stimulation of GIPR and GLP-1R may enhance insulin secretion and improve insulin sensitivity beyond the effect of selective GLP-1 receptor stimulation. Researchers studying incretin receptor crosstalk have used this compound as a reference tool for comparing unimolecular dual agonism against combination dosing of individual receptor-selective ligands.

Adipocyte Biology and Lipid Metabolism Research

Because GIPR is expressed in adipose tissue and GLP-1R is not, this dual agonist class provides researchers a molecular tool for studying GIPR-mediated adipocyte effects in isolation from confounding GLP-1R adipose signaling. Chronic GIPR agonism may modulate both fasted and postprandial adipocyte function differentially in the context of reduced and elevated insulin signaling, an area of active interest in preclinical lipid metabolism and macronutrient partitioning research.

Pancreatic Beta Cell and Islet Research

Within the pancreas, GIP and GLP-1 together promote beta cell proliferation and inhibit apoptosis, thereby expanding pancreatic beta cell mass in preclinical models. Researchers investigating islet biology, glucose-stimulated insulin secretion mechanisms, and beta cell survival pathways have used dual incretin agonists as in vitro tools for studying coordinated endocrine pancreas signaling.

Biased Signaling and Structure-Activity Research

The distinct signaling properties of this compound at the GLP-1 receptor — including imbalance toward GIP receptor engagement combined with biased GLP-1 receptor signaling — together account for a pharmacological profile that is of particular interest in comparative receptor pharmacology research. Structural biologists and pharmacologists have studied this compound class to characterize how sequence modifications at key residue positions shift receptor selectivity and downstream signaling bias.

 

Research Summary: What the Preclinical Science Shows

Research on 39-amino acid dual GIP/GLP-1 receptor agonist peptides spans endocrinology, adipocyte biology, structural pharmacology, and islet research. Preclinical studies across in vitro systems and animal models have contributed to a growing mechanistic literature. Below is a summary of key preclinical research areas.

Research AreaModelKey Findings
Insulin SecretionPancreatic islet modelsBiased GLP-1R agonism and GIPR co-activation studied for effects on glucose-stimulated insulin secretion in islet preparations. Beta-arrestin1 identified as a limiting factor for GLP-1 but not GIP or dual agonist-induced insulin response.
Adipose Tissue FunctionIn vitro adipocyte modelsGIPR agonism studied for direct modulation of adipocyte nutrient metabolism, lipolysis, and lipogenesis in preclinical models.
Beta Cell BiologyRodent and in vitro islet modelsGIP and GLP-1 receptor co-activation studied for effects on beta cell proliferation, apoptosis inhibition, and beta cell mass in animal models.
Receptor Occupancy and BiasIn vitro receptor binding assaysOccupancy analysis confirmed greater GIPR engagement than GLP-1R at equivalent doses. Biased GLP-1R signaling toward cAMP over beta-arrestin recruitment characterized in preclinical pharmacology studies.
Central Nervous System SignalingRodent modelsGIP and GLP-1 receptor distribution in appetite-regulatory brain regions studied in preclinical models of energy homeostasis.
Hepatic Lipid ResearchDiet-induced obesity animal modelsDual incretin receptor agonism studied for effects on hepatic fat content and liver function parameters in preclinical MASH models.

The body of preclinical research on dual GIP/GLP-1 receptor agonist peptides is well-developed relative to the broader triagonist literature. Larger, well-controlled studies remain necessary before any conclusions about translational mechanisms of action can be drawn.

Why Researchers Choose Azoth for Dual Regulator DIA-39-C20

Scientific rigor and product consistency are essential when working with structurally complex 39-amino acid acylated peptides. Azoth provides Dual Regulator DIA-39-C20 manufactured to strict purity specifications, backed by third-party certificate of analysis documentation for each batch.

  • Verified ≥99% purity via HPLC testing
  • USA-manufactured under strict quality protocols
  • Third-party tested for identity, purity, and stability
  • Lyophilized powder format for maximum shelf stability
  • Certificate of Analysis available for every batch

Whether your focus is dual incretin receptor pharmacology, adipocyte biology, or pancreatic islet signaling in animal models, Azoth provides the compound quality your laboratory research demands.

Storage and Handling

Dual Regulator DIA-39-C20 is supplied in lyophilized (freeze-dried) powder form. Store at 2–8°C in a cool, dry environment away from direct light and moisture. After reconstitution with bacteriostatic water, keep refrigerated and use in accordance with your laboratory research protocol. Stability is maintained for up to 24 months when stored correctly in lyophilized form.

Legal Disclaimer

Dual Regulator DIA-39-C20 sold by Azoth is supplied strictly for laboratory research and analytical purposes only and is not intended for human or veterinary use, diagnostic use, therapeutic use, metabolic use, weight-management use, hormone use, endocrine use, food use, cosmetic use, or personal use. This product has not been evaluated by the FDA and is not intended to diagnose, treat, cure, or prevent any disease or medical condition. Bodily introduction of any kind into humans or animals is strictly prohibited by law. All purchasers must be licensed researchers or qualified laboratory professionals. By purchasing this product, you acknowledge that you are aware of the applicable regulations in your jurisdiction and that you will use this compound exclusively within a qualified research environment.

Research FindingsJournalDataSource Link
1. Frias JP, et al. “Efficacy and safety of LY3298176, a novel dual GIP and GLP-1 receptor agonist, in patients with type 2 diabetes: a randomised, placebo-controlled and active comparator-controlled phase 2 trial.”Lancet.2018; 392(10160):2180-2193.https://pubmed.ncbi.nlm.nih.gov/30293770/
2. Coskun T, et al. “Tirzepatide modulates the regulation of adipocyte nutrient metabolism through long-acting activation of the GIP receptor.”Cell Metab.2024; 36(7):1534-1550.https://www.cell.com/cell-metabolism/fulltext/S1550-4131(24)00186-4
3. Willard FS, et al. “Tirzepatide is an imbalanced and biased dual GIP and GLP-1 receptor agonist.”JCI.2020; 130(9):4303-4306.https://pmc.ncbi.nlm.nih.gov/articles/PMC7526454/
4. Alexiadou K, Tan TM. “Targeting the incretin system in obesity and type 2 diabetes.”Compr. Physiol.2022; 12(3):3671-3710.https://pubmed.ncbi.nlm.nih.gov/35766834/
5. Coskun T, et al. “LY3298176, a novel dual GIP and GLP-1 receptor agonist for the treatment of type 2 diabetes mellitus and obesity.”Mol. Metab.2018; 18:3-14.https://pubmed.ncbi.nlm.nih.gov/30473097/
6. Min T, Bain SC. “The Role of Tirzepatide, Dual GIP and GLP-1 Receptor Agonist, in the Management of Type 2 Diabetes.”Diabetes Ther.2021; 12(1):143-157.https://pubmed.ncbi.nlm.nih.gov/33145709/
7. Rosenstock J, et al. “Efficacy and safety of a novel dual GIP and GLP-1 receptor agonist tirzepatide in patients with type 2 diabetes (SURPASS-1): a double-blind, randomised, phase 3 trial.”Lancet.2021; 398(10295):143-155.https://pubmed.ncbi.nlm.nih.gov/34186022/
8. Sun B, et al. “Structural basis of GLP-1 receptor and GIPR agonism by tirzepatide.”Nature.2022; 603(7901):525-529.https://pubmed.ncbi.nlm.nih.gov/35237831/
9. PubChem. “Tirzepatide, CID 156588324.”PubChem Compound Database.2022.https://pubchem.ncbi.nlm.nih.gov/compound/156588324
10. ClinicalTrials.gov. “Tirzepatide Once Weekly in Participants With Obesity or Overweight (SURMOUNT-1).”ClinicalTrials.gov.NCT04184622.https://clinicaltrials.gov/study/NCT04184622

What Is Dual Regulator DIA-39-C20?

Dual Regulator DIA-39-C20 is a synthetic 39-amino acid acylated peptide engineered from a GIP peptide backbone, designed for research into simultaneous activation of two distinct incretin receptor pathways: the glucose-dependent insulinotropic polypeptide receptor (GIPR) and the glucagon-like peptide-1 receptor (GLP-1R). With a molecular formula of C225H348N48O68 and a molecular weight of 4813.45 g/mol (CAS 2023788-19-2), this compound occupies a structurally distinct position from single-target GLP-1R agonists, incorporating modifications at key residues to enable balanced engagement of both receptor systems from a single molecular entity. Its structure is based on the GIP sequence and includes a C20 fatty diacid moiety that prolongs the duration of action through albumin binding, making it a relevant reference compound for researchers studying extended-half-life peptide pharmacokinetics alongside multi-receptor signaling. At Azoth, we offer Dual Regulator DIA-39-C20 synthesized to ≥99% purity, intended exclusively for licensed researchers and laboratory professionals.

How Does Dual Regulator DIA-39-C20 Work? Two Receptor Pathways Explored

Dual Regulator DIA-39-C20 is studied for an imbalanced and biased dual receptor profile, engaging the GIP receptor with greater occupancy than the GLP-1 receptor at equivalent concentrations. This receptor selectivity pattern makes it a useful tool for researchers seeking to isolate the relative contributions of each pathway in in vitro and animal model systems.

GIP Receptor Signaling

Receptor binding at the GIPR increases intracellular cyclic adenosine monophosphate (cAMP) in pancreatic beta cells, stimulating glucose-dependent insulin secretion. GIPR is widely expressed in islets, gut, adipose tissue, and brain, and GIP stimulates lipolysis and inhibits insulin-induced lipogenesis in adipocyte models. Researchers studying adipocyte nutrient metabolism have used this compound class as a tool for investigating how GIPR agonism modulates fat tissue function independently of GLP-1R signaling.

GLP-1 Receptor Signaling

Signaling studies demonstrate that this compound class shows bias at the GLP-1 receptor to favor cAMP generation over beta-arrestin recruitment, coincident with a weaker ability to drive GLP-1 receptor internalization compared with native GLP-1. GLP-1 receptors are distributed across the endocrine pancreas, heart, stomach, adipose tissue, vagus nerve, and various regions of the central nervous system, and animal studies have shown that GLP-1 promotes beta cell neogenesis and proliferation while inhibiting apoptosis.

Biased Agonism and Receptor Crosstalk

Experiments in primary pancreatic islets reveal that beta-arrestin1 limits the insulin response to GLP-1 but not to GIP or this dual agonist class, suggesting that the biased agonism profile may enhance insulin secretion in preclinical models. The imbalanced receptor engagement — greater GIP receptor occupancy combined with biased GLP-1 receptor signaling — creates a pharmacological profile distinct from selective GLP-1R agonists, offering researchers a model system for studying how these two pathways interact when co-activated simultaneously.

Adipose Tissue as a Direct Mechanistic Target

Adipose tissue is a potential direct mechanistic target of dual GIPR and GLP-1R agonists in contrast to GLP-1R monoagonists, since GIPR but not GLP-1R is expressed in adipose tissue. Preclinical and in vitro studies confirm the ability of GIPR/GLP-1R agonists to directly regulate adipose tissue function, illustrating modulation of adipocyte function as an important mechanistic target of this compound class.

 

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