GIP Specific Neutra™ Antibody Products

Are you grappling with prolonged drug development timelines or challenges in targeting metabolic regulators like GIP? Creative Biolabs' GIP-specific neutra™ antibody products overcome these hurdles through advanced hybridoma screening and epitope-specific engineering, empowering you to develop high-precision neutralizing antibodies that accelerate therapeutic discovery for diabetes and obesity.

Introduction to GIP

Gastric inhibitory polypeptide (GIP), a 42-amino acid incretin hormone, is secreted by intestinal K-cells in response to nutrient intake. Primarily known for its role in glucose homeostasis, GIP stimulates insulin secretion postprandially, modulates adipocyte lipid metabolism, and exerts pleiotropic effects on bone remodeling and neuronal signaling. Unlike glucagon-like peptide-1 (GLP-1), GIP exhibits dual regulatory roles in energy storage, contributing to its complex involvement in metabolic disorders.

• Structure

GIP's bioactive conformation is stabilized by α-helical domains spanning residues 7–28, critical for receptor binding. Its N-terminal region (amino acids 1–14) mediates interaction with the GIP receptor (GIPR), a class B G protein-coupled receptor (GPCR). Structural studies reveal that tyrosine residues at positions 10 and 13 are essential for maintaining binding affinity, while C-terminal truncations reduce biological activity.

• Related Signaling Pathways

GIP activates GIPR, triggering cAMP/PKA signaling in pancreatic β-cells and adipocytes. This pathway enhances glucose-dependent insulin secretion and promotes lipid storage via upregulation of lipoprotein lipase. Concurrently, GIPR signaling in the hypothalamus influences appetite regulation through mTOR pathway modulation. Paradoxically, chronic GIP overexposure in obesity induces receptor desensitization, contributing to insulin resistance—a phenomenon pivotal to metabolic dysfunction.

Fig. 1 Interaction of GIP and GIPRs.¹

• Associated Pathologies

Dysregulated GIP signaling is implicated in type 2 diabetes, obesity, and non-alcoholic fatty liver disease (NAFLD). Elevated GIP levels in obese individuals correlate with exacerbated adiposity and impaired insulin secretion, while GIPR antagonism demonstrates therapeutic potential in preclinical models.

Applications of GIP Neutralizing Antibodies

• Mechanistic Insights into Metabolic Dysregulation

GIP neutralizing antibodies enable researchers to investigate the hormone's tissue-specific effects. For instance, selective GIP blockade in murine models reveals its role in visceral fat expansion, while co-administration with GLP-1 analogs uncovers synergistic glucose-lowering effects.

• Therapeutic Development for Obesity

Preclinical studies demonstrate that neutralizing GIP activity reduces adipocyte hypertrophy and improves insulin sensitivity. Antibodies conjugated to Fc domains for extended half-life are being evaluated in primate models as monotherapies or combined with GLP-1 receptor agonists.

• Biomarker Discovery

Anti-GIP antibodies facilitate ultrasensitive ELISA-based quantification of circulating GIP, aiding in patient stratification for incretin-based therapies. Clinically, elevated GIP levels post-bariatric surgery correlate with sustained weight loss, highlighting its predictive value.

• Drug Resistance Profiling

Antibodies serve as critical tools to assess GIPR desensitization mechanisms in diabetic patients, informing the design of next-generation biased agonists or allosteric modulators.

Our Anti-GIP Neutralizing Antibody Products

Creative Biolabs delivers rigorously validated GIP-specific neutra™ antibody products to advance your metabolic disease research and therapeutic development. Our antibodies are optimized for specificity, scalability, and reproducibility across functional assays. The anti-GIP neutralizing antibodies are engineered to disrupt GIP-GIPR interactions with sub-nanomolar affinity. These antibodies feature:

-Epitope specificity: Target the N-terminal bioactive core (residues 1–14), ensuring precise blockade of receptor activation.

-Cross-reactivity: Validated against human, murine, and primate GIP isoforms.

-Functional validation: Demonstrated efficacy in inhibiting GIP-induced cAMP production in vitro and reducing fat accumulation in vivo.

Contact our scientific team today to explore custom solutions for your GIP-targeted projects.

REFERENCE

1. Pelle, Maria Chiara, et al. "Role of a dual glucose-dependent insulinotropic peptide (GIP)/glucagon-like peptide-1 receptor agonist (twincretin) in glycemic control: from pathophysiology to treatment." Life 12.1 (2021): 29. Distributed under Open Access license CC BY 4.0, without modification. https://doi.org/10.3390/life12010029