NP1192 |
Catalog No.GC80928
One-Click Copy Product Info
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NP1192 is a potent, selective PROTAC NAT10 degrader.
Products are for research use only. Not for human use. We do not sell to patients.
Cas No.: 2966791-41-1
Sample solution is provided at 25 µL, 10mM.
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In Vivo, NP1192 (25 mg/kg, i.p., every 2 days for a week) synergizes with anti-PD-L1 to inhibit tumor growth, suppress glycolysis, and enhance CD8+ Teff cell immunity in U14-luc xenograft mouse model[1].
In Vitro, NP1192 (0-20 μM, 24-48 h) induces NAT10 degradation in SiHa (human) and U14 (murine) CCa cell lines in a dose-and time-dependent manner, through the ubiquitin-proteasome system (UPS) rather than via lysosomal pathways[1]. NP1192 (36 h) inhibits cervical cancer (SiHa) cell growth with an IC50 of 7.814 μM (76.2 μM in resistant cells) and additionally shows dose-dependent efficacy in organoids, with IC50 values of 9.947, 3.048, and 13.76 μM for ovarian (OV), cervical (CESC), and glioblastoma (GBM) models, respectively[1]. NP1192 (20 μM, 0-72 h and 2 weeks) significantly reduces cell viability, induces cell cycle arrest, and suppresses invasion and clonogenic growth in CCa cells[1]. NP1192 (0.195-50 μM, 1-8 days) induces a pronounced reduction in organoid size and number across tumor models (ovarian, cervical, and glioblastoma), while the corresponding normal organoids remained unaltered, indicating minimal cytotoxicity to nonmalignant tissues[1]. NP1192 (20 μM, 36 h) reprograms the hypoxic tumor microenvironment (TME) and metabolism in CCa cells by degrading NAT10 and thereby impairing HIF-1α expression, which disrupts glycolysis as evidenced by reduced glucose uptake and lactate production alongside elevated ATP levels[1].
References:
[1]. Ao, K., et al. Targeted NAT10 Degradation by PROTAC NP1192 Suppresses Hypoxia-Adaptive Glycolysis and Reinvigorates CD8+ Effector T-Cell Function for Synergistic Cancer Immunotherapy. ACS Central Science. 2025.
[2]. Zhou Q, et al. PROTAC technology for sensitizing melanoma to immune checkpoint therapy[J]. Journal of Experimental & Clinical Cancer Research, 2026.
[3]. Xiong J, et al. Functional roles and mechanisms of NAT10-mediated RNA ac4C modification in normal development and cancer progression. Front Cell Dev Biol. 2026 Mar 6;14:1795359.
| Cas No. | 2966791-41-1 | SDF | |
| Formula | C39H42N8O5S | M.Wt | 734.87 |
| Solubility | DMSO: 100 mg/mL (136.08 mM; Need ultrasonic) | Storage | Store at -20°C |
| Shipping Condition | Evaluation sample solution: shipped with blue ice. All other sizes available: with RT, or with Blue Ice upon request. | ||
| Prepare stock solution | |||
|
1 mg | 5 mg | 10 mg |
| 1 mM | 1.3608 mL | 6.8039 mL | 13.6078 mL |
| 5 mM | 272.2 μL | 1.3608 mL | 2.7216 mL |
| 10 mM | 136.1 μL | 680.4 μL | 1.3608 mL |
Step 1: Enter information below (Recommended: An additional animal making an allowance for loss during the experiment)
g
μL
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Calculation results:
Working concentration: mg/ml;
Method for preparing DMSO master liquid: mg drug pre-dissolved in μL DMSO ( Master liquid concentration mg/mL, Please contact us first if the concentration exceeds the DMSO solubility of the batch of drug. )
Method for preparing in vivo formulation: Take μL DMSO master liquid, next addμL PEG300, mix and clarify, next addμL Tween 80, mix and clarify, next add μL saline, mix and clarify.
Method for preparing in vivo formulation: Take μL DMSO master liquid, next add μL Corn oil, mix and clarify.
Note: 1. Please make sure the liquid is clear before adding the next solvent.
2. Be sure to add the solvent(s) in order. You must ensure that the solution obtained, in the previous addition, is a clear solution before proceeding to add the next solvent. Physical methods such as vortex, ultrasound or hot water bath can be used to aid dissolving.
3. All of the above co-solvents are available for purchase on the GlpBio website.
Quality Control & SDS
- View current batch:
- Purity: >99.00% Appearance: A solid
- COA (Certificate of Analysis)
- SDS (Safety Data Sheet)
- Datasheet
Average Rating: 5 (Based on Reviews and 30 reference(s) in Google Scholar.)