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Targeted therapy! The Capetin Prize winning "Click Chemistry" can be used like this!Targeted therapy! The Nobel Prize winning "Click Chemistry" can be used like this!2025-02-06
1309 Results for "
PI3K-
" in MedChemExpress (MCE) Product Catalog:
Products (1309)
1309 Results for "PI3K-" in MCE Product Catalog:
Cat. No.: HY-N7695
CAS No.: 23133-56-4
Cat. No.: HY-W075770
CAS No.: 1313-99-1
Synonyms: Nickel monoxide
Target:
Environmental Pollutants Apoptosis Reactive Oxygen Species (ROS) Caspase TGF-beta/Smad p38 MAPK Akt PI3K
Research Areas:
Nickel(II) oxide (nickel monoxide) is a chemical warfare agent that can enter the body through the respiratory tract and other routes, distributing to organs such as the lungs and testes. The nanoparticle form of nickel(II) oxide (NiO NPs) exhibits antibacterial, anti-leishmanial, anti-diabetic, and anti-cancer activities. NiO NPs can be activated by ultraviolet and visible light, generating reactive oxygen species (ROS). Nickel(II) oxide induces oxidative stress by generating reactive oxygen species, activating the TGF-β1-mediated MAPK and PI3K/AKT pathways, disrupting the MMPs/TIMPs balance, and upregulating the expression of inflammatory factors (IL-1β, IL-6) and apoptosis-related molecules (Bax, caspase-3, p53), while inhibiting the activity of the anti-apoptotic molecule Bcl-2. Nickel(II) oxide induces cytotoxicity, promotes fibrosis, triggers inflammatory responses, and causes apoptosis. Nickel(II) oxide can be applied in research on the safety assessment of nanomaterials, such as in the context of pulmonary fibrosis and reproductive system toxicity [3].
Cat. No.: HY-108649
CAS No.: 1047980-83-5
Target:
P2Y Receptor G-quadruplex Phospholipase PKC Src CaMK PI3K Akt NO Synthase PERK Sodium Channel
Research Areas:
Cardiovascular Disease Neurological Disease Inflammation/Immunology Cancer
MRS2768 is a potent, selective, and metabolically stable P2Y2 receptor agonist with an EC50 of 1.89 μM for the human P2Y2 receptor. MRS2768 activates Gq/PLC/PKC signaling, leading to downstream phosphorylation of Akt, eNOS, and ERK, with effects varying by cell type. MRS2768 inhibits ENaC via Gq/PKC/Src/Akt to promote natriuresis and lower blood pressure in the kidney. MRS2768 activates eNOS to increase NO secretion in endothelial cells. MRS2768 drives proliferation via PI3K/Akt in fibroblasts and cancer cells. MRS2768 exerts anti-apoptotic effects through PKC/Src/Akt in cardiomyocytes. MRS2768 can be applied to investigate P2Y2-dependent pathological processes, including acute kidney injury, chronic kidney disease and renal fibrosis, DOCA-salt induced hypertension, myocardial infarction, pulmonary arterial hypertension, pancreatic cancer, cardiac fibrosis, dry eye disease, as well as shear stress-mediated vascular remodeling and atherosclerosis [3] .
Cat. No.: HY-116497
CAS No.: 1627843-95-1
PH11 is a novel focal adhesion kinase (FAK) inhibitor that rapidly induces apoptosis in TRAIL-resistant PANC-1 cells when combined with TRAIL, but has no effect on normal human fibroblasts. The study found that PH11 downregulates c-FLIP through inhibition of FAK and phosphatidylinositol-3-kinase (PI3K)/AKT pathways, thereby restoring the TRAIL apoptotic pathway, suggesting that this combination therapy may provide an attractive therapeutic strategy for the safe and effective treatment of pancreatic cancer. PH11 selectively inhibits c-FLIP expression by modulating upstream signaling pathways and may represent an innovative therapeutic strategy. Although further work is needed to fully elucidate the mechanism of PH11-induced TRAIL sensitization, we believe that our results will provide a new approach to target c-FLIP without the risk of interfering with caspase-8 processing, which could potentially lead to TRAIL resistance. This study also suggests a role for the FAK/AKT signaling pathway in regulating c-FLIP expression in TRAIL-induced apoptosis, and this understanding will provide important clues to control the resistance mechanism to optimize the potential of TRAIL-based pancreatic cancer treatment.
Cat. No.: HY-12017B
CAS No.: 1159490-85-3
Target:
PF-04217903 phenolsulfonate is an orally active, highly selective ATP-competitive c-Met kinase inhibitor with a Ki value of 4.8 nM and a Kd value of 4.5 nM. PF-04217903 phenolsulfonate blocks c-Met and HGF signaling pathways, inhibits MET phosphorylation, and blocks downstream MAPK, PI3K/AKT and PLCγ1 pathways. PF-04217903 phenolsulfonate suppresses tumor proliferation, survival, migration, invasion, angiogenesis and metastasis, induces apoptosis, and enhances efferocytosis, Annexin A1 expression and resolution of inflammation. PF-04217903 phenolsulfonate retains activity against several c-Met mutants (M1131T, V1220I, H1094R). PF-04217903 phenolsulfonate increases the incidence of subarachnoid hemorrhage and reduces survival rate without altering aneurysm formation, and also prevents lymph node metastasis induced by VEGF inhibition. PF-04217903 phenolsulfonate is applicable to research related to tumors (pancreas, stomach, lung, brain, colon, breast, kidney, melanoma, etc.), intracranial aneurysms and inflammatory diseases (gouty arthritis, neutrophilic pleuritis) [3] .
Cat. No.: HY-N2593R
CAS No.: 32507-66-7
Cat. No.: HY-W011927R
CAS No.: 80-09-1
Synonyms: Bisphenol S (Standard); Bis(4-hydroxyphenyl) sulfone (Standard)
Target:
P2Y Receptor G-quadruplex Phospholipase PKC Src CaMK PI3K Akt NO Synthase PERK Sodium Channel
Research Areas:
Cardiovascular Disease Neurological Disease Inflammation/Immunology Cancer
MRS2768 tetrasodium salt is a potent, selective, and metabolically stable P2Y2 receptor agonist with an EC50 of 1.89 μM for the human P2Y2 receptor. MRS2768 tetrasodium salt activates Gq/PLC/PKC signaling, leading to downstream phosphorylation of Akt, eNOS, and ERK, with effects varying by cell type. MRS2768 tetrasodium salt inhibits ENaC via Gq/PKC/Src/Akt to promote natriuresis and lower blood pressure in the kidney. MRS2768 tetrasodium salt activates eNOS to increase NO secretion in endothelial cells. MRS2768 tetrasodium salt drives proliferation via PI3K/Akt in fibroblasts and cancer cells. MRS2768 tetrasodium salt exerts anti-apoptotic effects through PKC/Src/Akt in cardiomyocytes. MRS2768 tetrasodium salt can be applied to investigate P2Y2-dependent pathological processes, including acute kidney injury, chronic kidney disease and renal fibrosis, DOCA-salt induced hypertension, myocardial infarction, pulmonary arterial hypertension, pancreatic cancer, cardiac fibrosis, dry eye disease, as well as shear stress-mediated vascular remodeling and atherosclerosis [3] .
Cat. No.: HY-174379
NTLiverTac PDE6D degrader-1 is a PDE6D NTLiverTac degrader with a DC50 of 4.09 μM. NTLiverTac PDE6D degrader-1 is formed by conjugating a PDE6D PROTAC degrader with the NTCP ligand Cholic acid (HY-N0324). NTLiverTac PDE6D degrader-1 triggers the ubiquitin-proteasome system-mediated degradation process by forming a complex with PDE6D and MDM2, inducing proteasome-dependent and NTCP-dependent degradation. NTLiverTac PDE6D degrader-1 inhibits PDE6D-dependent KRAS trafficking and suppresses KRAS-related oncogenic signaling cascades. NTLiverTac PDE6D degrader-1 inhibits the activation of the PI3K/AKT/mTOR signaling pathway and induces cellular Apoptosis. NTLiverTac PDE6D degrader-1 enters cancer cells via NTCP-mediated endocytosis. NTLiverTac PDE6D degrader-1 can be used in the research of hepatoblastoma (MDM2 ligand: (4R,5S)-Nutlin carboxylic acid (HY-128836); NTCP ligand: Cholic acid (HY-N0324); PDE6D ligand: Sorafenib (HY-10201)) .
Cat. No.: HY-18719S
CAS No.: 1584173-54-5
Target:
Research Areas:
Neurological Disease Metabolic Disease Inflammation/Immunology Cancer
Hyaluronic acid sodium (MW 200-1560) is a biopolymer composed of repeating disaccharide units, with a molecular weight of 200-1560. Hyaluronic acid sodium is a major component of the extracellular matrix (ECM). It is synthesized on the plasma membrane. Hyaluronic acid sodium exerts its effects by binding to receptors CD44 and RHAMM. Hyaluronic acid sodium activates PI3K-Akt signaling. Hyaluronic acid sodium also enhances cell invasion and angiogenesis by promoting or stimulating the binding of proteolytic MMP-9 to the cell surface. Elevated hyaluronic acid levels are associated with tumor cell growth, adhesion, migration, invasion, and angiogenesis in digestive system cancers. Hyaluronic acid sodium is involved in tissue remodeling and rapid cell proliferation in several physiological processes, including embryonic morphogenesis and wound healing. Hyaluronic acid sodium can be used as a regulator of cancer-associated lymphangiogenesis. Hyaluronic acid sodium can be used as a drug delivery carrier for sodium butyrate, enhancing its anti-proliferative activity against breast cancer cell lines. Hyaluronic acid sodium can lubricate the corneal endothelium. Hyaluronic acid sodium can improve tissue hydration and enhance the resistance of cells to mechanical damage. Hyaluronic acid sodium has been conjugated with antibodies to ensure that the active compound continues to exert its effects at the site of inflammation. Hyaluronic acid sodium can be used in research in the fields of osteoarthritis, ophthalmology, cosmetic dermatology, oncology, and liver diseases [3] .
Synonyms: Hyaluronan, low endotoxin; Hyaluronate, low endotoxin
Synonyms: Norcoclaurine (Standard); Demethyl-Coclaurine (Standard)
Cat. No.: HY-W015777R
CAS No.: 105-13-5
Synonyms: P-Methoxy-benzyl alcoho (Standard); (4-Methoxyphenyl)methanol (Standard)
Cat. No.: HY-L249
6,182 compounds
Protein lactylation, an emerging post-translational modification identified in recent years, plays a critical role in linking cellular metabolic reprogramming, epigenetic regulation, and signaling networks. Based on a systematic framework encompassing lactate metabolism, lactylation, and downstream signaling pathways, this compound library comprehensively targets multiple regulatory layers, including histone modification enzymes (such as p300 and HDACs), key glycolytic enzymes (such as PKM2, LDHA, and GAPDH), transcriptional regulators (such as STAT3, HMGB1, and p53), as well as central signaling pathway nodes including HIF-1α, NF-κB, and PI3K-AKT-mTOR. This integrated design enables a comprehensive representation of the regulatory roles of lactylation across the “metabolism–epigenetics–signaling” axis.
MCE has assembled a collection of 6,182 known bioactive compounds and potential functional molecules, making this library suitable for a wide range of applications, including high-throughput drug screening, inhibitor identification, and mechanistic studies. It can be used to systematically evaluate the functional roles of lactylation in biological processes such as tumor metabolism, immune regulation, and inflammatory responses, and to efficiently identify small-molecule candidates with regulatory potential, thereby facilitating the development of innovative therapeutics targeting the interplay between metabolism and epigenetic regulation.
Cat. No.: HY-15268
CAS No.: 1092787-12-6
PP487 is a selective dual inhibitor of Tyrosine kinase/PI3-K, with IC50 values of 0.017 μM, 0.072 μM, 0.004 μM, 0.01 μM, 0.55 μM, 0.22 μM, and < 0.01 μM against DNA-PK, mTOR, Hck, Src, EGFR, EphB4, and PDGFR, respectively. PP487 can be used in cancer research .
Cat. No.: HY-184703
Research Areas:
Antidiabetic agent 9 is an orally active antidiabetic agent. Antidiabetic agent 9 promotes the translocation of GLUT4 to the cell surface, activates the AMPK signaling pathway, and has no effect on the PI-3-K/AKT signaling pathway. Antidiabetic agent 9 reduces blood glucose levels in Streptozotocin (HY-13753)-induced diabetic rats. Antidiabetic agent 9 can be used in the research of diabetes .
Cat. No.: HY-RS10523
Target:
Research Areas:
PIK3CA Human Pre-designed siRNA Set A contains three designed siRNAs for PIK3CA gene (Human), as well as a negative control, a positive control, and a FAM-labeled negative control.
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Protocols
Targeted therapy! The Capetin Prize winning "Click Chemistry" can be used like this!Targeted therapy! The Nobel Prize winning "Click Chemistry" can be used like this!A suitable model is crucial in drug screening experiments. Organs can mimic the three-dimensional functional structure of internal organs, have similar spatial organization to corresponding organs, maintain some key characteristics, and reproduce some physiological functions. They are widely used for modeling and personalized drug screening physiological functions.2025-02-06
