UcallM® DRUG-seq Library Prep Kit

UcallM® DRUG-seq Library Prep Kit is designed for rapid transcriptome profiling of scarce cells or tissue specimens. Valid for 1 000-10 000 input cells, it allows direct cell-lysis-to-library workflow without RNA extraction, thus avoiding nucleic-acid loss. Unique barcode-plus-UMI design enables pooled multiplex library construction and accurate mRNA quantification to counteract PCR amplification bias. Thanks to low-sample-input requirements, batch-processing capability and cost-effectiveness, this kit is widely applied in drug screening, tumor tracing and organoid research.

Experimental Workflow

Key Advantages 1.Low-cell-input compatibility: works with 1 000-10 000 cells; suitable for multiple cell types and organoid models 2.Integrated barcode + UMI for multiplex-pooled library construction and precise molecular-counting, enabling cost-efficient high-throughput sequencing 3.Direct cell lysis without RNA purification; simplified workflow reduces batch-to-batch variation Applications 1.Drug discovery & screening (target identification, compound efficacy assessment etc.) 2.Mechanistic research on tumor pathogenesis and biomarker discovery 3.Stem-cell and organoid biology 4.Gene-function investigation Customer Publications Aging Dis. NeuroD1 enhances AAV-PHP.eB transduction via endothelial reprogramming and mediates multi-target repair after ischemic stroke (DOI:10.14336/AD.2023.1213).

Fig. 1-11. (D) Volcano plot of differentially expressed genes (DEGs) between the NeuroD1-treated group and the control group; (E) NeuroD1-regulated DEGs were enriched in biological processes such as phagocytosis. Use-Cases 1.Cell Stem Cell. iPSC-derived venous-endothelial-cell modeling of vascular malformations and drug-repurposing discovery (DOI:10.1016/j.stem.2024.10.015).

Figure 1-12. In this study, DRUG-seq combined with deep learning models was applied for high-throughput drug screening on iVEC carrying TIE2 mutation. By analyzing transcriptomic changes in drug-treated cells, potential drugs capable of reversing the VM phenotype and bringing the transcriptome of mutant cells closer to wild-type cells were identified.

2.Oncogene. Mycobacterium tuberculosis suppresses METTL14-dependent Nox2 mRNA m⁶A methylation via EsxB to impair anti-tuberculosis immunity (DOI:10.1038/s41388-025-03309-z). This study integrated single-cell ATAC-seq and single-cell RNA-seq, combined with CRISPRi, ATAC-seq and DRUG-seq technologies, to explore the regulatory mechanism underlying all-trans retinoic acid (ATRA)-induced differentiation of PML/RARα⁺ acute promyelocytic leukemia (APL) NB4 cell line.

Figure 1-13. Herein, DRUG-seq was used for high-throughput analysis of transcriptomic effects induced by overexpression of SPI1 and/or CEBPE in NB4, HL60 and K562 cells. It revealed that these transcription factors, either individually or synergistically, activate granulocyte-related genes, confirming their capacity to trigger partial differentiation programs in the absence of ATRA.