SU 16f
(Synonyms: SU16F) 目录号 : GC12686SU 16f是一种有效的酪氨酸激酶抑制剂，可抑制VEGF-R2、FGF-R1和PDGFRβ，IC50值分别为0.14、2.29和0.01μM。
Cas No.:251356-45-3
Sample solution is provided at 25 µL, 10mM.
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SU 16f is a potent tyrosine kinase inhibitor that inhibits VEGF-R2, FGF-R1, and PDGFRβ, with IC50 values of 0.14, 2.29, and 0.01μM, respectively [1]. SU 16f can inhibit PDGFRβ phosphorylation, resulting in a significant reduction in the phosphorylation of ERK1/2 and STAT3, while the expression of CLDN1 decreased[2]. SU 16f has been widely used as a model compound for molecular docking to analyze the characteristic sites and develop a series of related receptor tyrosine kinase inhibitors[3].
In vitro, SU 16f pretreatment (20μM) for 8 hours significantly inhibited the promoting effect of gastric cancer-derived mesenchymal stem cell (GC-MSC) conditioned medium on the cell proliferation and migration of SGC-7901 cells[4]. SU 16f treatment (5μM; 14 days) eliminated the inhibitory effects of PDGF-BB on BMP2-induced osteogenic differentiation of primary periosteum-derived progenitor cells (PDCs)[5]. Treatment with 10μM SU 16f for 72 hours significantly inhibited the migration of mouse brain vascular pericytes (MBVP) induced by PDGFβ[6].
In vivo, SU 16f administration (2mg/kg/day) via intraperitoneal injection for five consecutive days restored the formation of beige adipose tissue in tamoxifen (TMX)-induced Sma-CreERT2; R26-mTmG male mice exposed to cold environment[7]. Intrathecal injection of a 10μl 3mM SU 16f solution (dissolved in 0.1M PBS containing 3% DMSO) at a rate of 1μl/4s, administered daily for eight consecutive days, blocked the PDGFRβ pathway, inhibited fibrotic scar formation, and promoted axonal regeneration and motor function recovery after spinal cord injury in mice[8].
References:
[1] Sun L, Tran N, Liang C, et al. Design, synthesis, and evaluations of substituted 3-[(3-or 4-carboxyethylpyrrol-2-yl) methylidenyl] indolin-2-ones as inhibitors of VEGF, FGF, and PDGF receptor tyrosine kinases[J]. Journal of medicinal chemistry, 1999, 42(25): 5120-5130.
[2] Pang S, Wu R, Lv W, et al. Use of a pH-responsive imatinib mesylate sustained-release hydrogel for the treatment of tendon adhesion by inhibiting PDGFRβ/CLDN1 pathway[J]. Bioactive Materials, 2024, 38: 124-136.
[3] Kammasud N, Boonyarat C, Tsunoda S, et al. Novel inhibitor for fibroblast growth factor receptor tyrosine kinase[J]. Bioorganic & medicinal chemistry letters, 2007, 17(17): 4812-4818.
[4] Huang F, Wang M, Yang T, et al. Gastric cancer-derived MSC-secreted PDGF-DD promotes gastric cancer progression[J]. Journal of cancer research and clinical oncology, 2014, 140(11): 1835-1848.
[5] Wang X, Matthews B G, Yu J, et al. PDGF modulates BMP2‐induced osteogenesis in periosteal progenitor cells[J]. JBMR plus, 2019, 3(5): e10127.
[6] Li Z, Zheng M, Yu S, et al. M2 macrophages promote PDGFRβ+ pericytes migration after spinal cord injury in mice via PDGFB/PDGFRβ pathway[J]. Frontiers in Pharmacology, 2021, 12: 670813.
[7] Benvie A M, Lee D, Steiner B M, et al. Age-dependent Pdgfrβ signaling drives adipocyte progenitor dysfunction to alter the beige adipogenic niche in male mice[J]. Nature Communications, 2023, 14(1): 1806.
[8] Li Z, Yu S, Liu Y, et al. SU16f inhibits fibrotic scar formation and facilitates axon regeneration and locomotor function recovery after spinal cord injury by blocking the PDGFRβ pathway[J]. Journal of Neuroinflammation, 2022, 19(1): 95.
SU 16f是一种有效的酪氨酸激酶抑制剂，可抑制VEGF-R2、FGF-R1和PDGFRβ，IC50值分别为0.14、2.29和0.01μM [1]。SU 16f能抑制PDGFRβ磷酸化，从而导致ERK1/2和STAT3磷酸化显著减少，同时CLDN1表达降低[2]。SU 16f已被广泛用作分子对接的模型化合物，用于分析特征位点并开发一系列相关的受体酪氨酸激酶抑制剂[3]。
在体外，用SU 16f（20μM）预处理8小时，能显著抑制胃癌来源间充质干细胞条件培养基对SGC-7901细胞增殖和迁移的促进作用[4]。SU 16f处理（5μM；14天）消除了PDGF-BB对BMP2诱导的原代骨膜来源祖细胞（PDCs）成骨分化所产生抑制作用[5]。用10μM SU 16f处理72小时，显著抑制了PDGFβ诱导的小鼠脑血管周细胞(MBVP)的迁移[6]。
在体内，连续五天通过腹腔注射SU 16f（2mg/kg/day），恢复了暴露于寒冷环境的他莫昔芬(TMX)诱导的Sma-CreERT2; R26-mTmG雄性小鼠中米色脂肪组织的形成[7]。连续8天每天以1μl/4s的速率髓鞘内注射10μl的3mM SU 16f溶液（溶于含3% DMSO的0.1M PBS中）可阻断PDGFRβ通路抑制纤维化瘢痕形成，促进小鼠脊髓损伤后轴突再生和运动功能恢复[8]。
| Cell experiment [1]: | |
Cell lines | Primary periosteum-derived progenitor cells (PDCs) |
Preparation Method | Primary PDCs were seeded in 12-well plates and cultured in growth medium for 7 days to differentiate into osteoblasts (with 50μg/ml ascorbic acid and 4mM β-glycerophosphate sodium). Starting from the 7th day, recombinant human bone morphogenetic protein 2 (BMP2) and recombinant rat platelet-derived growth factor-BB (PDGF-BB) were added respectively, and the culture was continued for 14 days in the presence or absence of SU 16f (5μM). The growth factor-containing medium was replaced every 2 days, and alkaline phosphatase (ALP) staining was performed. |
Reaction Conditions | 5μM; 14 days |
Applications | SU 16f treatment eliminated the inhibitory effects of PDGF-BB on BMP2-induced osteogenic differentiation of PDCs. |
| Animal experiment [2]: | |
Animal models | Sma-CreERT2; R26-mTmG male mice |
Preparation Method | Sma-CreERT2; R26-mTmG male mice (12 months old) were housed in the animal room, with a light/dark cycle of 14:10 hours, and had free access to food and water. The TMX (50mg/kg) dissolved in sunflower oil was intraperitoneally injected into the mice for two consecutive days, and then the mice were raised at room temperature for 7 days. Subsequently, on each of the following 5 days, the vehicle (5% DMSO) and SU 16f (2mg/kg/day) were injected intraperitoneally, respectively. Then, the mice were placed in a refrigerated box at 6.5°C for 7 days, and the fat tissues of the mice were collected for analysis. |
Dosage form | 2mg/kg/day for 5 days; i.p. |
Applications | SU 16f treatment restored beige fat formation in aged mice exposed to a cold environment. |
References: | |
| Cas No. | 251356-45-3 | SDF | |
| 别名 | SU16F | ||
| 化学名 | (E)-3-(2,4-dimethyl-5-((2-oxo-6-phenylindolin-3-ylidene)methyl)-1H-pyrrol-3-yl)propanoic acid | ||
| Canonical SMILES | O=C1NC2=CC(C3=CC=CC=C3)=CC=C2/C1=C\C4=C(C)C(CCC(O)=O)=C(C)N4 | ||
| 分子式 | C24H22N2O3 | 分子量 | 386.44 |
| 溶解度 | DMSO: <100mM | 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。 |
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| 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 | |||
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1 mg | 5 mg | 10 mg |
| 1 mM | 2.5877 mL | 12.9386 mL | 25.8772 mL |
| 5 mM | 517.5 μL | 2.5877 mL | 5.1754 mL |
| 10 mM | 258.8 μL | 1.2939 mL | 2.5877 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。
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Quality Control & SDS
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- Purity: >99.50%
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