mTOR Activator

L-Leucine-d₁₀ is the deuterium labeled L-Leucine. L-Leucine is an essential branched-chain amino acid (BCAA), which activates the mTOR signaling pathway.

L-Leucine-¹⁵N is the ¹⁵N-labeled L-Leucine. L-Leucine is an essential branched-chain amino acid (BCAA), which activates the mTOR signaling pathway.

Salidroside (Standard) is the analytical standard of Salidroside. This product is intended for research and analytical applications. Salidroside (Rhodioloside) is a prolyl endopeptidase inhibitor. Salidroside alleviates cachexia symptoms in mouse models of cancer cachexia via activating mTOR signalling. Salidroside protects dopaminergic neurons by enhancing PINK1/Parkin-mediated mitophagy.

Orcinol glucoside is an orally active, blood-brain barrier permeable osteoblast proliferation promoter that targets the Nrf2/Keap1, mTOR and p38 signaling pathways. Orcinol glucoside promotes Nrf2 nuclear translocation, upregulates antioxidant enzyme levels, enhances the phosphorylation of mTOR and p70S6K, and inhibits the enzymatic activity of HAS2 as well as the nuclear translocation of GR. Orcinol glucoside also alleviates oxidative stress, inhibits autophagic flux, osteoclastogenesis and TGF-β1-induced M2 polarization, while reducing collagen deposition and effectively promoting the proliferation, differentiation and mineralization of osteoblasts. Orcinol glucoside also exhibits anti-pulmonary fibrosis, anxiolytic and antidepressant activities. Orcinol glucoside can be used in the research of senile and glucocorticoid-induced osteoporosis, idiopathic pulmonary fibrosis (IPF), anxiety and other related diseases.

Tetrahydroalstonine ((-)-Tetrahydroalstonine) is an indole alkaloid and a selective α₂-adrenergic receptor antagonist. Tetrahydroalstonine exhibits certain neuroprotective effects. Tetrahydroalstonine can regulate autophagy-lysosomal function by activating the Akt/mTOR pathway, significantly reducing OGD/R-induced primary cortical neuronal injury.

Perfluoroundecanoic acid is a perfluoroalkyl substance (PFAS). Perfluoroundecanoic acid is an orally active oxidative stress inducer. Perfluoroundecanoic acid promotes macrophage M2 polarization, activates Wnt/β-catenin signaling and enhances β-catenin nuclear accumulation. Perfluoroundecanoic acid -induced M2 phenotype macrophage accelerates tumor progression in vitro and in vivo. Perfluoroundecanoic acid induces DNA damage, reproductive and pathophysiological dysfunctions via oxidative stress in male Swiss mice. Perfluoroundecanoic acid inhibits Leydig cell development in pubertal male rats via inducing oxidative stress and autophagy. Perfluoroundecanoic acid accelerates insulitis development in a mouse model of type 1 diabetes. Perfluoroundecanoic acid can be used for the study of ovarian cancer, type 1 diabetes and inflammation.

Flavokawain C is an orally active natural chalcone. Flavokawain C inhibits the proliferation of various cancer cells. Flavokawain C upregulates GADD153 in cancer cells, inhibits the phosphorylation of Akt and JNK, suppresses early ERK phosphorylation, activates late ERK phosphorylation, activates caspase related subtypes, induces PARP-1 cleavage, causes upregulation of p21 and p27, downregulation of mutant p53 and anti-apoptotic IAP proteins, elevates intracellular ROS levels, reduces SOD activity, and induces apoptosis. Flavokawain C downregulates FABP4, induces autophagy in cancer cells, and activates the AMPK/mTOR pathway. Flavokawain C decreases the expression of glycolysis-related proteins GLUT1 and HK2, and inhibits glycolysis in nasopharyngeal carcinoma cells. Flavokawain C inhibits the activation of the EGFR/PI3K/Akt/mTOR signaling pathway and reduces the expression of HSP90B1. Flavokawain C inhibits angiogenesis by decreasing the expression of angiogenic proteins Ang-1 and VEGF in human umbilical vein endothelial cells. Flavokawain C increases γ-H2AX levels in cells, inhibits the phosphorylation of FAK, PI3K and AKT in cells, and induces DNA damage in cells. Flavokawain C exerts anti-tumor activity in multiple tumor xenograft mouse models. Flavokawain C is applicable to research related to colorectal cancer, colon adenocarcinoma, nephroblastoma, nasopharyngeal carcinoma and liver cancer.

(2S,6S)-Hydroxynorketamine hydrochloride is a neurorelaxant with potential antidepressant and analgesic effects. (2S,6S)-Hydroxynorketamine hydrochloride can activate the mTOR pathway, increase the phosphorylation level of downstream targets, and antagonize α7-nicotinic acetylcholine receptor (nAChR) to exert neuroactive properties.

Tripotassium hydroxycitrate is an orally active, multi-target, multi-bioactive organic acid. Tripotassium hydroxycitrate activates Nrf2 and its downstream molecule GPX4, increases glutathione levels, and thereby inhibits ferroptosis. Tripotassium hydroxycitrate activates the Nrf2/Keap1 and ACLY/NF-κB signaling pathways, upregulates the activities of antioxidant enzymes such as superoxide dismutase, reduces MDA content, thereby alleviating oxidative stress and renal tubular epithelial cell apoptosis, and improves pulmonary vascular and right ventricular remodeling. Tripotassium hydroxycitrate activates both the AMPK and mTORC1/S6K pathways, triggers the unfolded protein response, arrests the cancer cell cycle, and induces DNA fragmentation.

Psicose (DL-Psicose) is an orally effective sugar substitute. Psicose activates the PI3K/Akt/mTOR pathway to promote muscle synthesis. Psicose upregulates IGF-1 and downregulates Myostatin. Psicose normalizes mitochondrial dysfunction by increasing G6P activity. Psicose enhances the activity of antioxidant enzymes and reduces oxidative stress markers. Psicose increases muscle mass, grip strength and muscle weight in aged mice and diet-induced obese mice. Psicose improves obesity and type 2 diabetes. Psicose can be used in the research of age-related sarcopenia.

PI5P4Kγ-IN-1 is an ATP-competitive, highly selective chemical probe for PI5P4Kγ, with a K_d of 19 nM and an IC₅₀ of 67 nM. PI5P4Kγ-IN-1 effectively inhibits PI5P4Kγ function and activates the mTORC1 signaling pathway in cells. PI5P4Kγ-IN-1 can be used in studies related to diseases such as breast cancer.

NEO214 is an autophagy inhibitor and a covalent conjugate of the PDE4 inhibitor Rolipram (HY-16900) and perillyl alcohol (HY-N7000). It has anti-cancer activity and blood-brain barrier (BBB) permeability. Over sex. NEO214 prevents autophagy-lysosome fusion, thereby blocking autophagic flux and triggering glioma cell death. The process involves mTOR activation, andTFEB(Transcription Factor EB) aggregation. NEO214 inhibitionMacroautophagy/autophagy in glioblastoma cells has the potential to overcome chemotherapy resistance in glioblastoma.

L-Leucine-d₇ is the deuterium labeled L-Leucine. L-Leucine is an essential branched-chain amino acid (BCAA), which activates the mTOR signaling pathway.

Arjunolic acid is an orally active, multifunctional bioactive compound. Arjunolic acid exhibits free radical scavenging activity, as well as fungal and bacterial activities. Arjunolic acid induces apoptosis (Apoptosis) in various cancer cells. Arjunolic acid protects hepatocytes against induced oxidative stress and apoptosis by reducing reactive oxygen species and inhibiting NF-κB activation. Arjunolic acid regulates pancreatic dysfunction in type 2 diabetic rats by blocking the activation of the TLR-4/MyD88 and canonical Wnt pathways. Arjunolic acid inhibits neuroinflammation and ameliorates depressive behaviors via the SIRT1/AMPK/Notch1 signaling pathway in microglia. Arjunolic acid improves Crohn's disease-like colitis by restoring gut microbiota composition and inhibiting TLR4 signaling. Arjunolic acid suppresses osteosarcoma progression by inhibiting Wnt3a-mediated M2 polarization of macrophages. Arjunolic acid ameliorates diabetic retinopathy via the autophagy pathway regulated by AMPK/mTOR/HO-1. Arjunolic acid is applicable to research related to type 2 diabetes, organ toxicity, depression, Crohn's disease, osteosarcoma, diabetic retinopathy, and testicular dysfunction.

Ginsenoside C-K (Standard) is the analytical standard of Ginsenoside C-K. This product is intended for research and analytical applications. Ginsenoside C-K, a bacterial metabolite of G-Rb1, exhibits anti-inflammatory effects by reducing iNOS and COX-2. Ginsenoside C-K exhibits an inhibition against the activity of CYP2C9 and CYP2A6 in human liver microsomes with IC50s of 32.0±3.6 μM and 63.6±4.2 μM, respectively.

L-Leucine-2-¹³C,¹⁵N is the ¹³C- and ¹⁵N-labeled L-Leucine. L-Leucine is an essential branched-chain amino acid (BCAA), which activates the mTOR signaling pathway.

L-Leucine-d₂ is the deuterium labeled L-Leucine. L-Leucine is an essential branched-chain amino acid (BCAA), which activates the mTOR signaling pathway.

L-Leucine-¹⁸O₂ is the ¹⁸O-labeled L-Leucine. L-Leucine is an essential branched-chain amino acid (BCAA), which activates the mTOR signaling pathway.

Ganglioside GT1b (porcine) ammonium is a member of the ganglioside family. Ganglioside GT1b (porcine) ammonium acts as a protective signal against nerve injury-induced spinal synapse elimination. Ganglioside GT1b (porcine) ammonium induces HA synthesis and the phosphorylation of Akt/mTOR in orbital fibroblasts. Ganglioside GT1b (porcine) ammonium enhances porcine oocyte maturation and induces activation of EGFR and ERK1/2 signaling. Ganglioside GT1b (porcine) ammonium is a putative host cell receptor for the Merkel cell polyomavirus. Ganglioside GT1b (porcine) ammonium can be used for the researches of cancer, infection, immunology, endocrinology and neurological disease, such as Thyroid eye disease.

PF-4455242 hydrochloride is an orally bioavailable, blood-brain barrier-permeable κ-opioid receptor (KOR) inhibitor. PF-4455242 hydrochloride blocks in vivo effects induced by KOR and MOR agonists, and elicits KOR-independent outward currents in ventral tegmental area neurons. PF-4455242 hydrochloride promotes energy expenditure and activates the hypothalamic mTOR pathway. PF-4455242 hydrochloride attenuates stress-induced behavioral effects and produces antidepressant-like effects. PF-4455242 hydrochloride can be used in studies related to pain, depression, addictive disorders, and obesity induced by estrogen withdrawal.