myoblasts

(±)-1,2-Diolein (1,2-Dioleoyl-rac-glycerol) 是一种PKC 激活剂，可以增加肌小管 Ca2+内流。

NVS-SM2 is an effective small molecule splicing enhancer of SMN2 with oral activity. NVS-SM2 showed increased exon 7 inclusion and upregulated SMN protein expression in SMA fibroblasts and SMN cells Δ7 5025 mouse myoblasts.

1(R)-(Trifluoromethyl)oleyl alcohol is an analog of oleic acid .1It inhibits ferroptosis induced by erastin in primary fibroblasts isolated from patients with Friedreich ataxia, a neuro- and cardiodegenerative disorder characterized by loss or impaired activity of frataxin (FXN), when used at concentrations of 5, 10, or 20 μM. 1(R)-(Trifluoromethyl)oleyl alcohol (5 μM) reduces lipid peroxidation induced byFXNsiRNA knockdown in NBT human myoblasts. 1.Cotticelli, M.G., Forestieri, R., Xia, S., et al.Identification of a novel oleic acid analog with protective effects in multiple cellular models of Friedreich ataxiaACS Chem. Neurosci.11(17)2535-2542(2020)

22(S)-hydroxy Cholesterol is a synthetic oxysterol and a modulator of the liver X receptor (LXR). [1] t prevents monocyte chemoattractant protein 1 (MCP-1) expression induced by the LXR agonist GW 3965 in primary hepatocytes and downregulates mRNA expression of the LXR target genes CD36, ACSL1, and SCD-1 in human myotubes. It decreases triacylglycerol and diacylglycerol synthesis from labeled palmitate and acetate, respectively, in human myoblasts by 50% when used at a concentration of 10 uM. 22(S)-hydroxy Cholesterol also reduces fatty acid synthase (FAS) reporter activity through an LXR response element in the promoter region in COS-1 cells transfected with RXRα and LXRα and decreases the expression of MCP-1 and CCR2 in a mouse model of chronic ethanol consumption.[1] [2] Dietary supplementation of 22(S)-hydroxy cholesterol (30 mg kg per day) leads to less body weight gain and lower liver triacylglycerol levels in rats when fed either a regular chow or high-fat diet as well as prevents an increase in plasma triacylglycerol levels resulting from a high-fat diet.[3]

AZT triphosphate TFA (3'-Azido-3'-deoxythymidine-5'-triphosphate TFA) is a active triphosphate metabolite of Zidovudine (AZT). AZT triphosphate TFA exhibits antiretroviral activity and inhibits replication of HIV. AZT triphosphate TFA also inhibits the DNA polymerase of HBV. AZT triphosphate TFA activates the mitochondria-mediated apoptosis pathway[1][2][3]. Treatment with 100 μM Zidovudine (AZT) for 48h disrupts the mitochondrial tubular network via accumulation of AZT triphosphate (AZT-TP) in H9c2 cells. AZT triphosphate accumulation causes downregulation of Opa1 and upregulation of Drp1. AZT triphosphate causes mitochondrial dysfunction, increases the production of cytotoxic reactive oxygen species (ROS), and impairs the balance of the mitochondrial quality control system in H9c2 cell model established from rat embryonic myoblasts[1]. [1]. Ryosuke Nomura, et al. Azidothymidine-triphosphate Impairs Mitochondrial Dynamics by Disrupting the Quality Control System. Redox Biol. 2017 Oct;13:407-417. [2]. Takeya Sato, et al. Engineered Human tmpk/AZT as a Novel Enzyme/Prodrug Axis for Suicide Gene Therapy. Mol Ther. 2007 May;15(5):962-70. [3]. K Y Hostetler, et al. Enhanced Oral Absorption and Antiviral Activity of 1-O-octadecyl-sn-glycero-3-phospho-acyclovir and Related Compounds in Hepatitis B Virus Infection, in Vitro. Biochem Pharmacol. 1997 Jun 15;53(12):1815-22.

Beauverolide Ka 是一种环四缩酚肽，是 Beauveria bassiana 真菌的代谢产物。Beauverolide Ka 浓度为 50 μM 时可刺激培养的大鼠 L6 成肌细胞的葡萄糖摄取。Beauverolide Ka 在 10 μM 时表现出对 HEI-OC1 细胞的保护作用，并且在 L6 成肌细胞和肌管中表现出剂量依赖性活性。

BML-278 是一种 SIRT1 激活剂 ，EC150 值为 1 μM。BML-278 增加父本和母本原核中的 H3K9 甲基化并抑制 H3K9 乙酰化，可用于改善早期胚胎发育。BML-278 促使原代人间充质细胞的细胞周期停止在 G1 S 期，可用于延缓衰老。BML-278 减少 U937 细胞中的微管蛋白乙酰化，增加小鼠 C2C12 成肌细胞的线粒体密度。

PTP1B AKR1B1-IN-1是一种针对PTP1B和AKR1B1的双重抑制剂，其IC50值分别为0.06 μM和4.3 μM。该化合物也能抑制TC-PTP，IC50为9 μM。在小鼠成肌细胞中，PTP1B AKR1B1-IN-1作为胰岛素模拟剂使用，并能减少AKR1B1依赖的山梨醇积累，有助于抑制2型糖尿病的发展并控制血糖水平。

PTP1B AKR1B1-IN-2（化合物7f）是一种双重PTP1B AKR1B1抑制剂，具有IC50：3.2和2.1 μM，Ki：4.0和0.9μM。该化合物作为胰岛素模拟剂，能够改善小鼠C2C12肌母细胞的葡萄糖摄取，并可用于2型糖尿病（T2DM）的研究。

INF 195 是一种炎性小体 NLRP3 抑制剂，抑制 NLRP3 驱动的巨噬细胞焦亡 和 IL-1β 释放。INF 195 可减轻异丙肾上腺素诱导的 H9c2 大鼠成肌细胞肥大，可用于研究心肌缺血和心肌梗死。

Muscle homing peptide M12 主要结合于肌肉细胞表面蛋白,且能促进肌母细胞对纳米颗粒(NPs)的摄取.该肽通过 N-羟基琥珀酰亚胺酯反应,于其 N-末端α-氨基基团与PLGA-PEG纳米颗粒形成共价连接.

T9 peptide (SKTFNTHPQSTP) 是一种特定肌肉靶向的肽.它与 C2C12 成肌细胞具有高度结合能力.当T9 peptide 与寡核苷酸结合时,其对心脏和股四头肌的靶向特异性得到增强,但对肾、肝和膈肌的靶向作用不明显.

Pep1-DNP conjugate 9 是由 DNP-半抗原与 FGFR1 结合肽构成的功能化肽，对 FGFR1 具有良好的亲和力，KD 为 5.01 μM。它能将抗 DNP 抗体募集到 FGFR1 阳性细胞表面，抑制 FGF2 诱导的骨骼成肌细胞增殖，并诱导细胞凋亡 (apoptosis)。在小鼠模型中，Pep1-DNP conjugate 9 展现出抗肿瘤活性。