Akt Activator

Bisphenol F is an orally active endocrine disruptor. Bisphenol F promotes ROS generation, upregulates p-AKT/p-GSK3β, and induces Apoptosis. Bisphenol F interferes with glucose metabolism, affects neurodevelopment and reproductive function. Bisphenol F reduces social novelty preference in mouse offspring. Bisphenol F can be used in bone, blood, and fat-related studies. Bisphenol F is used as a substitute for Bisphenol A (HY-18260).

Suberic acid (Octanedioic acid) is an orally active crystalline dibasic acid. Suberic acid activates the Akt signaling pathway and regulates the expression of molecules related to the TGF-β and MAPK signaling pathways. Suberic acid inhibits skin dryness.

L-Valine-¹³C₅ ((S)-Valine-¹³C₅) is the ¹³C-labeled L-Valine (HY-N0717). L-Valine ((S)-Valine) is a nonlinear semiorganic material. L-Valine causes lipid peroxidation and accumulation of malondialdehyde (MDA), exhibits inhibitory activity against cyanobacteria. L-Valine inhibits multidrug-resistant bacteria through activation of PI3K/Akt signaling pathway and inhibition of arginase.

SY-LB-35 is a potent bone morphogenetic protein (BMP) receptor agonist. SY-LB-35 can stimulate significant increases in cell number and cell viability in the C2C12 myoblast cell line, and causes shifts towards the S and G2/M phases of the cell cycle. SY-LB-35 stimulates canonical Smad and non-canonical PI3K/Akt, ERK, p38 and JNK intracellular signaling pathways.

Protectin D1, a neuroprotectin D1 produced by neuronal cells, is a member of a newly discovered family of bioactive products derived from docosahexaenoic acid. Protectin D1 also serves as a specialized pro-resolving mediator, exhibiting effective in vivo pro-resolving activity in various human disease models. Additionally, Protectin D1 is an inhibitor of NALP3 inflammasomes and regulates the PI3K/AKT and HIF-1α signaling pathways. Protectin D1 exerts anti-inflammatory effects by reducing ROS levels, inhibiting the expression of NALP3, ASC, and Caspase-1, and consequently decreasing the release of pro-inflammatory cytokines IL-1β and IL-18. Furthermore, Protectin D1 enhances miRNA-210 expression, activates the PI3K/AKT signaling pathway, and exerts cardioprotective effects. Protectin D1 holds promise for research in cardiovascular diseases and inflammatory disorders.

Doxepin Hydrochloride is an orally active, blood-brain barrier penetrant tricyclic antidepressant with multiple activities including hypnosis, sedation, analgesia and vasodilation. Doxepin Hydrochloride enhances the expression of PSD-95 and synapsin 1 via the PI3K/AKT/mTOR signaling pathway, and is metabolized to DesmethylDoxepin Hydrochloride in vivo. Doxepin Hydrochloride can be used in research related to various diseases such as depression, anxiety, obesity and atopic dermatitis.

Pam2CSK4 TFA is a TLR2 agonist. Pam2CSK4 TFA induces the expression of iNOS and NO in macrophage cell lines via TBK1 and MyD88 molecules. Pam2CSK4 TFA activates the NF-κB and Bruton's tyrosine kinase signaling pathways in platelets, and promotes platelet-endothelial cell interactions. TLR2 activation triggered by Pam2CSK4 TFA expands myeloid-derived suppressor cells (MDSCs) and suppresses anti-tumor immune responses in the tumor microenvironment. Pam2CSK4 TFA acts as a Th2-polarizing adjuvant in mouse vaccine models against Leishmania major and Brugia malayi. Pam2CSK4 TFA can be used in the research of various diseases, including thromboinflammatory diseases, sepsis, atherosclerosis, heart failure, influenza, lymphoma, melanoma, cutaneous leishmaniasis and lymphatic filariasis.

D927 (DS11252927) is an orally active glucose transporter type 4 (GLUT4) translocation activator with an EC₅₀ of 0.14 μM. D927 enhances the binding affinity of PI3Kα catalytic subunit p110α to canonical RAS proteins (KRAS4A, KRAS4B) and RRAS, RRAS2, MRAS. D927 activates the PI3Kα-AKT pathway (increasing phosphorylation of AKT, p70S6 kinase) without affecting the RAF-ERK1/2 pathway. D927 improves hyperglycemia in type 1 and type 2 diabetes mice model. D927 can be used for the study of glucose homeostasis disorders and diabetes.

ERBB agonist-1 is a ERBB4 agonist with an EC₅₀ of 10.5 μM. ERBB agonist-1 enhances NRG1-induced ERBB4 homodimerization and activates the PI3K/Akt and MAPK/ERK signaling pathways. ERBB agonist-1 acts as a cell survival promoter, anti-hypertrophic agent, anti-fibrotic agent, and cardioprotective agent. ERBB agonist-1 is applicable to the research of heart failure.

Vaccarin is an orally active flavonoid glycoside with multiple biological functions. Vaccarin promotes neovascularization by activating AKT and ERK. Vaccarin activates the AMPK signaling pathway to improve insulin resistance and steatosis. Vaccarin is a MAPK, NF-κB, and NFAT inhibitor, effectively blocking RANKL-induced osteoclastogenesis.

Histamine phosphate is the agonist for histamine receptor and a vasodilator. Histamine phosphate is an organic nitrogen compound that participates in local immune responses, regulates intestinal physiological functions, and acts as a neurotransmitter. Histamine phosphate affects p38 MAPK/Akt signaling pathway, exhibits antitumor, antioxidant and anti-inflammatory activities. Histamine phosphate can be used in the research of acute myeloid leukemia, malignant melanoma, and renal cell carcinoma.

YJ1206 is an orally active selective CDK12/CDK13 PROTAC degrader. YJ1206 induces DNA damage and genomic instability, activates the AKT pathway, and triggers apoptosis. YJ1206 reduces tumor cell viability, inhibits tumor growth, and attenuates tumor cell dissemination. YJ1206 is applicable to research related to prostate cancer and high-grade serous tubo-ovarian cancer.

L-Valine (Standard) ((S)-Valine (Standard)) is the analytical standard of L-Valine (HY-N0717). This product is intended for research and analytical applications. L-Valine ((S)-Valine) is a nonlinear semiorganic material. L-Valine causes lipid peroxidation and accumulation of malondialdehyde (MDA), exhibits inhibitory activity against cyanobacteria. L-Valine inhibits multidrug-resistant bacteria through activation of PI3K/Akt signaling pathway and inhibition of arginase.

2,6-Dimethoxy-1,4-benzoquinone is a 1,4-benzoquinone derivative. 2,6-Dimethoxy-1,4-benzoquinone promotes phosphorylation of AKT, S6K, mTOR, 4E-BP1, and AMPK, and attenuates mTORC1 activity as part of the AKT/mTOR pathway. 2,6-Dimethoxy-1,4-benzoquinone stimulates myoblast differentiation, increases myotube size, elevates MHC protein expression, enhances mitochondrial biogenesis, respiration, and DNA content, and increases skeletal muscle weights, fiber size, grip strength, and treadmill performance. 2,6-Dimethoxy-1,4-benzoquinone exerts anti-cancer, anti-inflammatory, anti-adipogenic, antibacterial, and antimutagenic effects, inhibits adipogenic transcription factors, nitric oxide production, skin tumor development, Magnaporthe oryzae growth, spore germination, appressorium formation, and growth of select bacterial species, induces H₂O₂ generation and rice defense gene expression, and reduces rice blast lesion formation. 2,6-Dimethoxy-1,4-benzoquinone can be used for the research of obesity, skin tumorigenesis, rice blast disease, and food-borne illness.

Ginsenoside F2 is an orally active bioactive compound that participates in the regulation of metabolism and inflammation. Ginsenoside F2 promotes the phosphorylation of AMPK and ACC, binds to PPARγ, inhibits the phosphorylation of MAPK, activates the PI3K/AKT/GSK-3β pathway, reduces GLRX expression, and regulates lipid metabolism. Ginsenoside F2 reduces ROS production and MDA levels, restores SOD activity in cells, and alleviates oxidative stress. Ginsenoside F2 induces cell apoptosis (Apoptosis) and increases the number of cleaved caspase-3-positive cells. Ginsenoside F2 reduces body weight gain, adipose tissue weight and serum lipid levels in obese mice, and activates the hepatic AMPK signaling pathway and the expression of antioxidant enzymes. Ginsenoside F2 alleviates atopic dermatitis in mice by inhibiting inflammation and reshaping the gut microbiota. Ginsenoside F2 is applicable to research related to insulin resistance, obesity, atopic dermatitis, liver cancer, glioblastoma and glioma.

N-Oleoyl glycine is a lipoamino acid, which stimulates adipogenesis associated with activation of CB1 receptor and Akt signaling pathway in 3T3-L1 adipocyte.

Indoprofen ((±)-Indoprofe) activates AKT-AMPK signaling pathway, inhibits NF-κB/MAPK signaling pathway. Indoprofen exhibits anti-inflammatory and immunomodulatory activities. Indoprofen is orally active.

Ponicidin (Rubescensine B) is an orally active RIPK1 inhibitor with a K_d value of 135 nM. Ponicidin inhibits the JAK2/STAT3 pathway to induce apoptosis, activates the PI3K/Akt pathway, upregulates SIRT1 expression, alleviates oxidative stress, suppresses inflammatory responses and necroptosis, and blocks cell cycle progression. Ponicidin induces ROS production to exert antiproliferative and antiviral effects, while also improving cognitive function and reducing Aβ plaque deposition. Ponicidin can be used in studies related to hepatocellular carcinoma, Alzheimer's disease, and gastric cancer.

1,3-Dicaffeoylquinic acid is a caffeoylquinic acid derivative that exhibits antioxidant activity and radical scavenging activity.

Triphenyl phosphate is an orally active, blood-brain barrier-permeable aryl organophosphate flame retardant and endocrine disruptor. Triphenyl phosphate disrupts mitochondrial dynamic balance through oxidative stress, induces excessive mitophagy and apoptosis, and ultimately leads to myocardial fibrosis. In the brain, Triphenyl phosphate activates the NF-κB inflammatory pathway by disrupting the gut microbiota, alters tryptophan metabolism and elevates neurotoxins, thereby inducing anxiety- and depression-like behaviors. In the skeletal and reproductive systems, Triphenyl phosphate inhibits osteoblast differentiation and induces germ cell apoptosis by suppressing the MAPK/ERK pathway and activating the JNK signal, respectively. In adipose and placental tissues, Triphenyl phosphate promotes lipid accumulation by activating the PI3K/AKT-PPARγ axis, and disrupts placental metabolism via the MAOA/ROS/NF-κB cascade, impairing neurodevelopment of offspring.