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Development of a novel peripherally acting alpha2A- adrenergic receptor antagonist for anti-diabetic

GSE304258 Mus musculus (mouse) RNA-seq (gene expression) 2 samples Submitted 2026/08/01 Platform GPL24247
At a glance

RNA-seq (gene expression) · mouse · 2 samples

What it is
RNA-seq (gene expression)Gene activity measured by sequencing. The summary does not mention single-cell work, so this is most likely bulk: one average per sample, the usual starting point for comparing groups.
Organism
Mus musculus (mouse)
Samples
2 samples
Data you can get
A processed table (series matrix) and supplementary files from NCBI; the raw sequencing reads from ENA. Which of these hold counts depends on the study, so check the file list.
Summary (written by the submitters)
Studies have consistently highlighted the role of the alpha2A-adrenergic receptor (α2AAR) in the pathophysiology of type 2 diabetes (T2D), particularly its contribution to impaired insulin release and β-cell dysfunction. Yohimbine, a potent α2AAR antagonist, has shown therapeutic potential for T2D by improving insulin release, but its clinical application has been limited by central nervous system (CNS) side effects.
Read the full summary ↓
In this study, we developed a novel, peripherally acting α2AAR antagonist (CDS479-2) using molecular docking analysis and a bioisosteric replacement strategy applied to yohimbine`s structure. cryo-EM structures of α2AAR bound to either yohimbine or CDS479-2 confirm the molecular basis of α2AAR antagonism, validate our docking models, and reveal key ligand-receptor interactions for future drug design. Importantly, animal studies demonstrated that acute administration of CDS479-2 effectively lowered blood glucose and improved glucose tolerance in diabetic mice, without central side effects such as anxiety or blood pressure elevation commonly associated with α2AAR antagonism. Remarkably, once-daily administration of CDS479-2 for 2 weeks resulted in sustained normoglycemia and increased pancreatic β-cell density in diet-induced obese (DIO) mice, with upregulation of key genes involved in β-cell maturation and proliferation. These findings suggest that CDS479-2 represents a promising new approach for the treatment of T2D. Furthermore, the strategy we employed here may serve as a model for optimization for other drugs that with both peripheral and central targets.
This dataset
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Download · which file do I need?

Direct links to NCBI and ENA, no account and no request form. Pick by what you want to do: take the small processed table to look, the supplementary files to re-analyse, or the original raw data to start over.

1 · Just have a look

Processed table

The series matrix: one table of values per sample as the submitters processed it. The smallest download, and it opens in Excel or R. Start here to see what the data look like.

Series matrix ↓
2 · Re-analyse it

Supplementary files

The count tables and other files the authors uploaded. Take only the samples you need, or the whole study as GSE304258_RAW.tar (it can run to tens of gigabytes).

All supplementary files ↗ Whole study · RAW.tar ↓
3 · Start from the raw reads

Raw sequencing reads

The original FASTQ files, straight from the sequencer, held at ENA. Large, and you align them yourself, so only choose this if you need to re-process the study from scratch.

Raw reads on ENA ↗

What the files usually look like: For RNA-seq the counts are usually a table among the supplementary files (look for 'counts', 'expression', 'FPKM' or 'TPM' in the file name). The series matrix of a sequencing study is sometimes nearly empty.

Also filed as BioProject PRJNA1299786 and SRA study SRP605739. Searching any of these in the dataset finder brings you back here.

NCBI GEO page ↗
Samples in this study

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