NGI-1
(Synonyms: ML414) 目录号 : GC33055
NGI-1 (ML414)是一种有效的寡糖基转移酶（OST）抑制剂。
Cas No.:790702-57-7
Sample solution is provided at 25 µL, 10mM.
_1-3.$$$39978408@51.jpg');)
_1-9.$$$38538795@65.jpg');)
_1-9.$$$39112701@51.jpg');)
_1-7.$$$37316672@70.jpg');)
_366-372.$$$36198801@70.jpg');)
.$$$38565142@65.jpg');)
_1867-1883.$$$33248023@67.jpg');)
_eads6055.$$$39977546@45.jpg');)
_eadm9805.$$$40080571@45.jpg');)
_eadj3020.$$$39666821@45.jpg');)
_1-20.$$$39757301@28.jpg');)
_1-24.$$$38898113@28.jpg');)
_273-287.$$$36806353@46.jpg');)
_1-16.$$$37156877@44.jpg');)
_1-19.$$$37460805@44.jpg');)
_1291-1307.$$$34518654@46.jpg');)
NGI-1 (ML414) is an effective oligosaccharyl transferase (OST) inhibitor [1]. NGI-1 selectively inhibits the STT3A and STT3B subunits in the oligosaccharyl transferase (OST) complex, thereby blocking the N-linked glycosylation process of proteins [2-3]. NGI-1 is often used to study the regulation of glycosylation-dependent proteins such as EGFR in tumor cells and has certain anti-tumor potential [4].
In PC9 cells, NGI-1 (10μM; 48h) reduced the proliferation of both parental and T790M-expressing PC9 cell lines by approximately 90% [5]. In HEK293 cells, NGI-1 (5μM; 60min) treatment results in cell type-dependent dysfunction of HSV-1 [2]. In Caco2 cells, NGI-1 (1μM, 5μM; 3d) has a significant inhibitory effect on SARS-CoV-2 [6]. In SKMG3 cells, NGI-1 (10μM; 48h) disrupts RTK signaling in glioblastoma cells [7].
In oral squamous cell carcinoma xenograft model, combined inhibition of EREG glycosylation by targeting NGI-1 (10mg/kg; ip; 14d) significantly enhanced the efficacy of anti-PDL1 inhibitors in vivo [8]. In lung adenocarcinoma xenograft model, the tumor volume and wet weight of NGI-1 (20mg/kg; ip; 24d) treated mice were significantly smaller than those of the DMSO control group at the end point [9]. In CD24-WT nude mice, NGI-1 (20mg/kg; ip; 24d) treatment significantly inhibited tumor growth [10].
References:
[1]. Rinis N, Golden JE, Marceau CD, et al. Editing N-glycan site occupancy with small-molecule oligosaccharyltransferase inhibitors. Cell chemical biology. 2018 Oct 18; 25(10): 1231-1241.
[2]. Lu H, Cherepanova NA, Gilmore R, et al. Targeting STT3A-oligosaccharyltransferase with NGI-1 causes herpes simplex virus 1 dysfunction. The FASEB Journal. 2019 Feb 27;33(6):6801.
[3]. Harada Y, Ohkawa Y, Kizuka Y, et al. Oligosaccharyltransferase: a gatekeeper of health and tumor progression. International journal of molecular sciences. 2019 Dec 2; 20(23): 6074.
[4]. Cao Y, Yi W, Zhu Q. Glycosylation in the tumor immune response: the bitter side of sweetness: Glycosylation in the tumor immune response. Acta Biochimica et Biophysica Sinica. 2024 Jun 28; 56(8): 1184.
[5]. Lopez Sambrooks C, Baro M, Quijano A, et al. Oligosaccharyltransferase inhibition overcomes therapeutic resistance to EGFR tyrosine kinase inhibitors. Cancer research. 2018 Sep 1; 78(17): 5094-5106.
[6]. Huang YJ, Zhao H, Huang X, et al. Identification of oligosaccharyltransferase as a host target for inhibition of SARS-CoV-2 and its variants. Cell Discovery. 2021 Nov 30; 7(1): 116.
[7]. Baro M, Lopez Sambrooks C, Quijano A, et al. Oligosaccharyltransferase inhibition reduces receptor tyrosine kinase activation and enhances glioma radiosensitivity. Clinical Cancer Research. 2019 Jan 15; 25(2): 784-795.
[8]. Xu S, Wang H, Zhu Y, et al. Stabilization of EREG via STT3B-mediated N-glycosylation is critical for PDL1 upregulation and immune evasion in head and neck squamous cell carcinoma. International Journal of Oral Science. 2024 Jul 1; 16(1): 47.
[9]. Cheng J, Xia L, Hao X, et al, Tavolari S. Targeting STT3A produces an anti-tumor effect in lung adenocarcinoma by blocking the MAPK and PI3K/AKT signaling pathway. Translational Lung Cancer Research. 2022 Jun; 11(6): 1089.
[10]. Wang J, Zhang HM, Zhu GH, et al. STT3-mediated aberrant N-glycosylation of CD24 inhibits paclitaxel sensitivity in triple-negative breast cancer. Acta Pharmacologica Sinica. 2025 Apr; 46(4): 1097-1110.
NGI-1 (ML414)是一种有效的寡糖基转移酶（OST）抑制剂 [1]。NGI-1选择性抑制寡糖基转移酶（OST）复合物中的STT3A和STT3B亚基，从而阻断蛋白质的N-连接糖基化过程 [2-3]。NGI-1常用于研究肿瘤细胞中EGFR等糖基化依赖性蛋白的调控，具有一定的抗肿瘤潜力 [4]。
在PC9细胞中，NGI-1（10μM；48h）使亲本和表达T790M的PC9细胞系的增殖降低了约90% [5]。在HEK293细胞中，NGI-1（5μM；60分钟）处理导致细胞类型依赖性的HSV-1功能障碍 [2]。在Caco2细胞中，NGI-1（1μM，5μM；3d）对SARS-CoV-2有显著的抑制作用 [6]。在SKMG3细胞中，NGI-1（10μM；48h）可破坏胶质母细胞瘤细胞中的RTK信号传导 [7]。
在口腔鳞状细胞癌异种移植模型中，靶向NGI-1（10mg/kg；ip；14d）联合抑制EREG糖基化可显著增强抗PDL1抑制剂的体内疗效 [8]。在肺腺癌异种移植模型中，NGI-1（20mg/kg；ip；24d）治疗组小鼠的肿瘤体积和湿重在终点时均显著小于DMSO对照组 [9]。在CD24-WT裸鼠中，NGI-1（20mg/kg；ip；24d）治疗显著抑制肿瘤生长 [10]。
| Cell experiment [1]: | |
Cell lines | PC9 cells |
Preparation Method | Growth rates were determined by CellTiter 96 NonRadioactive Cell Proliferation Assay (Promega) according to the manufacturer's directions. Briefly, NSCLC cells (2 × 103) untreated or treated with 10μM NGI-1, 100μM gefitinib, or 1μM osimertinib were seeded in triplicate in 96-wells plates and grown in culture medium containing 10% serum. The media were changed with or without new inhibitor every 48 hours. |
Reaction Conditions | 10μM; 48h |
Applications | NGI-1 reduced the proliferation of both parental and T790M-expressing PC9 cell lines by approximately 90%. |
| Animal experiment [2]: | |
Animal models | Oral squamous cell carcinoma xenograft model |
Preparation Method | NGI-1 was diluted with 10% DMSO + 40% PEG300 + 5% Tween 80 + 45% saline to a final concentration of 1mg/mL, and the PDL1 inhibitor was diluted with PBS to a final concentration of 0.5mg/mL. In animal experiments, SPF female C57BL/6 mice (6 weeks old) were used. MTCQ1 cells were used to establish a tumor xenograft model, and cells (5×106 cells/100μL PBS) were subcutaneously injected into the flank of mice, and tumor size was monitored 3 times a week. NGI-1 and PDL1 inhibitors were administered by abdominal injection 4 times a week at doses of 10mg/kg and 5mg/kg, respectively. |
Dosage form | 10mg/kg; ip; 14d |
Applications | Combined inhibition of EREG glycosylation by targeting NGI-1 significantly enhanced the efficacy of anti-PDL1 inhibitors in vivo. |
References: | |
| Cas No. | 790702-57-7 | SDF | |
| 别名 | ML414 | ||
| Canonical SMILES | O=C(NC1=NC=C(C)S1)C2=CC(S(=O)(N(C)C)=O)=CC=C2N3CCCC3 | ||
| 分子式 | C17H22N4O3S2 | 分子量 | 394.51 |
| 溶解度 | DMSO : 160 mg/mL (405.57 mM) | 储存条件 | Store at -20°C |
| General tips | 请根据产品在不同溶剂中的溶解度选择合适的溶剂配制储备液；一旦配成溶液，请分装保存，避免反复冻融造成的产品失效。 储备液的保存方式和期限：-80°C 储存时，请在 6 个月内使用，-20°C 储存时，请在 1 个月内使用。 为了提高溶解度，请将管子加热至37℃，然后在超声波浴中震荡一段时间。 |
||
| Shipping Condition | 评估样品解决方案：配备蓝冰进行发货。所有其他可用尺寸：配备RT，或根据请求配备蓝冰。 | ||
| 制备储备液 | |||
 |
1 mg | 5 mg | 10 mg |
| 1 mM | 2.5348 mL | 12.6739 mL | 25.3479 mL |
| 5 mM | 0.507 mL | 2.5348 mL | 5.0696 mL |
| 10 mM | 0.2535 mL | 1.2674 mL | 2.5348 mL |
| 第一步：请输入基本实验信息（考虑到实验过程中的损耗，建议多配一只动物的药量） | ||||||||||
| 给药剂量 | mg/kg |  |
动物平均体重 | g | |
每只动物给药体积 | ul | |
动物数量 | 只 |
| 第二步：请输入动物体内配方组成（配方适用于不溶于水的药物；不同批次药物配方比例不同，请联系GLPBIO为您提供正确的澄清溶液配方） | ||||||||||
| % DMSO % % Tween 80 % saline | ||||||||||
| 计算重置 | ||||||||||
计算结果:
工作液浓度： mg/ml；
DMSO母液配制方法： mg 药物溶于 μL DMSO溶液（母液浓度 mg/mL，
体内配方配制方法：取 μL DMSO母液，加入 μL PEG300，混匀澄清后加入μL Tween 80，混匀澄清后加入 μL saline，混匀澄清。
1. 首先保证母液是澄清的；
2.
一定要按照顺序依次将溶剂加入，进行下一步操作之前必须保证上一步操作得到的是澄清的溶液，可采用涡旋、超声或水浴加热等物理方法助溶。
3. 以上所有助溶剂都可在 GlpBio 网站选购。
Quality Control & SDS
- View current batch:
- Purity: >99.50%
- COA (Certificate Of Analysis)
- SDS (Safety Data Sheet)
- Datasheet