myoblasts

(±)-1,2-Diolein [1,2-Dioleoyl-rac-glycerol] is a PKC activator that can increase Ca²⁺ influx in myotubes.

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, a cyclotetradepsipeptide derived from the Beauveria bassiana fungus, enhances glucose absorption in rat L6 myoblasts cultured at a concentration of 50 μM and exhibits protective effects on HEI-OC1 cells at 10 μM. It demonstrates dose-dependent activities in both L6 myoblasts and myotubes [1] [2].

BML-278 is a SIRT1 activator with an EC150 of 1 μM. It increases H3K9 methylation and inhibits H3K9 acetylation in parental and maternal prokaryotes, improving early embryonic development. BML-278 induces cell cycle arrest at the G1 S phase in primary human mesenchymal stromal cells, delaying senescence. It also reduces microtubule protein acetylation in U937 cells and increases mitochondrial density in mouse C2C12 myoblasts.

PTP1B AKR1B1-IN-1 is a dual inhibitor targeting protein tyrosine phosphatase 1B (PTP1B) and aldose reductase (AKR1B1), with IC50s of 0.06 μM for PTP1B and 4.3 μM for AKR1B1. It also inhibits T-cell protein tyrosine phosphatase (TC-PTP) with an IC50 of 9 μM. This compound acts as an insulin-mimetic in murine myoblasts, reduces AKR1B1-mediated sorbitol accumulation, and aids in managing blood glucose levels and inhibiting type 2 diabetes mellitus (T2DM) development [1].

PTP1B AKR1B1-IN-2 (Compound 7f) is a potent inhibitor targeting both PTP1B and AKR1B1 with IC50 values of 3.2 and 2.1 μM, respectively, and K i values of 4.0 and 0.9 μM. This compound acts as an insulin mimetic and enhances glucose uptake in murine C2C12 myoblasts, making it useful for Type 2 diabetes mellitus (T2DM) research [1].

INF 195 is an inflammasome NLRP3 inhibitor that inhibits NLRP3-driven macrophage pyroptosis and IL-1β release. INF 195 reduces isoproterenol-induced hypertrophy in H9c2 rat myoblasts and can be used to study myocardial ischemia and myocardial infarction.

Muscle homing peptide M12 preferentially binds to proteins on the surface of muscle cells. It enhances the cellular uptake of nanoparticles (NPs) in myoblasts. Additionally, Muscle homing peptide M12 is covalently attached to PLGA-PEG nanoparticles through an N-hydroxysuccinimide ester reaction, with the bonding occurring at the α-amino group at the N-terminus of the peptide chain.

T9 peptide (SKTFNTHPQSTP) is a muscle-targeting peptide that tightly binds to C2C12 myoblasts. When combined with oligonucleotides, T9 peptide enhances specificity towards the heart and quadriceps without similarly targeting the kidney, liver, or diaphragm.

Pep1-DNP conjugate 9 is a functionalized peptide composed of a DNP-hapten and an FGFR1-binding peptide. It exhibits good affinity for FGFR1, with a dissociation constant (KD) of 5.01 μM. This compound effectively recruits anti-DNP antibodies to the surface of FGFR1-positive cells, inhibits FGF2-induced proliferation of rat skeletal myoblasts, and induces apoptosis. In mouse models, Pep1-DNP conjugate 9 demonstrates antitumor activity.