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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-N0259R
CAS No.: 110623-73-9
Synonyms: Epmedin B (Standard)
Cat. No.: HY-N0392
CAS No.: 882664-74-6
Cat. No.: HY-N0565AR
CAS No.: 10592-13-9
Research Areas:
Infection Neurological Disease Inflammation/Immunology Cancer
Doxycycline hydrochloride (Standard) is the analytical standard of Doxycycline hydrochloride (HY-N0565A). This product is intended for research and analytical applications. Doxycycline hydrochloride is an orally active highly lipophilic, tissue-permeable MMP inhibitor with broad-spectrum antibacterial activity. Doxycycline hydrochloride is also a semi-synthetic antibiotic with chelating properties, which blocks bacterial protein synthesis and inhibits extracellular matrix degradation through interactions with zinc and calcium atoms. Doxycycline hydrochloride also inhibits mitochondrial biogenesis, translation, and the expression of respiratory chain proteins. Doxycycline hydrochloride induces apoptosis, inhibits autophagy and EMT, downregulates stem cell markers, and activates the PI3K-AKT pathway, thereby effectively inhibiting the viability and proliferation of cancer cells such as breast cancer cells. Doxycycline hydrochloride also promotes the survival and self-renewal of embryonic stem cells and neural stem cells, and reduces the frequency of medium changes in culture. Doxycycline hydrochloride has been applied in studies related to breast cancer, prostate cancer, bladder cancer, and other cancers [3] .
Cat. No.: HY-N0565AS
Research Areas:
Infection Neurological Disease Inflammation/Immunology Cancer
Doxycycline (Standard) is the analytical standard of Doxycycline (HY-N0565). This product is intended for research and analytical applications. Doxycycline is an orally active highly lipophilic, tissue-permeable MMP inhibitor with broad-spectrum antibacterial activity. Doxycycline is also a semi-synthetic antibiotic with chelating properties, which blocks bacterial protein synthesis and inhibits extracellular matrix degradation through interactions with zinc and calcium atoms. Doxycycline also inhibits mitochondrial biogenesis, translation, and the expression of respiratory chain proteins. Doxycycline induces apoptosis, inhibits autophagy and EMT, downregulates stem cell markers, and activates the PI3K-AKT pathway, thereby effectively inhibiting the viability and proliferation of cancer cells such as breast cancer cells. Doxycycline also promotes the survival and self-renewal of embryonic stem cells and neural stem cells, and reduces the frequency of medium changes in culture. Doxycycline has been applied in studies related to breast cancer, prostate cancer, bladder cancer, and other cancers [3] .
Cat. No.: HY-N0565S3
CAS No.: 1902958-13-7
Cat. No.: HY-N0657R
CAS No.: 63902-38-5
Cat. No.: HY-N0735R
CAS No.: 104112-82-5
Cat. No.: HY-N19029
CAS No.: 21871-10-3
Cat. No.: HY-N2942
CAS No.: 52328-96-8
Cat. No.: HY-N4246R
CAS No.: 382148-47-2
Cat. No.: HY-P6292
CAS No.: 2724212-01-3
Research Areas:
Cat. No.: HY-W274807
CAS No.: 4921-82-8
Research Areas:
TM-2-51 is a HDAC8 activator with a Kd value of 0.28 μM. TM-2-51 inhibits α-glucosidase with an IC50 of 171.21 μM. TM-2-51 upregulates HDAC8 expression, modulates the TP53, STAT3/ERK and PI3K-AKT pathways, alleviates LeTx-induced cell cycle arrest, downregulates JMJD3 and increases H3K27me3 levels. TM-2-51 selectively induces apoptosis in tumor cell and upregulates p53/p21 expression. TM-2-51 inhibits tumor cell proliferation, migration and invasion, induces G1-phase arrest and suppresses tumor growth in vivo. TM-2-51 can be used in research on osteosarcoma, anthrax, type 2 diabetes and neuroblastoma [3] .
Cat. No.: HY-W778236
CAS No.: 1346603-47-1
Synonyms: SAN 9789-13C,d3
Research Areas:
Norflurazon- 13C,d3 (SAN 9789- 13C,d3) is the d3, 13C-labeled Norflurazon (HY-114849). Norflurazon (SAN 9789) is a pre-emergence Herbicide. Norflurazon non-competitively inhibits phytoene desaturase by competing with the enzyme cofactor and disrupts carotenoid biosynthesis, thereby leading to chlorophyll photodegradation and chlorosis. Norflurazon inhibits MGDG synthase, CDP-choline phosphotransferase, Omega-3 FAD7 desaturase, and PG delta-3-trans desaturase, and activates LysoPC-acyltransferase and Omega-3 FAD3 desaturase. Norflurazon inhibits photosynthetic membrane organization, mitochondrial respiration, ATP production, PI3K signaling, and ERK1/2 phosphorylation. Norflurazon activates MAPK P38 phosphorylation and ER stress signaling. Norflurazon induces morphological malformations and cardiovascular effects in zebrafish embryos [3] .
Cat. No.: HY-RS10532
Target:
Research Areas:
PIK3CG Human Pre-designed siRNA Set A contains three designed siRNAs for PIK3CG gene (Human), as well as a negative control, a positive control, and a FAM-labeled negative control.
Cat. No.: HY-113720
CAS No.: 1041469-97-9
Target:
CDK Apoptosis Caspase Reactive Oxygen Species (ROS) JNK MDM-2/p53 Bcl-2 Family IGF-1R PI3K PKC Ras Akt
Research Areas:
RKS262 is an orally active cyclin/CDK inhibitor. RKS262 is also an apoptosis inducer and cell cycle regulator, exhibiting cytotoxic activity against cancer cells. RKS262 induces caspase-3 cleavage, ROS generation, SAPK/JNK activation, and upregulates the expression of p53, Bid, Bad, Bok, and p27. RKS262 inhibits the expression of Bcl-2, Mcl-1, Bcl-xL, p21, cyclin D1, cyclin B1, cdc-2, cyclin D4, and DNA-pk KU-80 subunit. RKS262 suppresses the phosphorylation of the IGF-1R/PI3K/PKC pathway, ras oncogene activity, and Cdk-6, while increasing total Akt expression. RKS262 induces G2/M or S phase cell cycle arrest, disrupts mitochondrial transmembrane potential, and reduces tumor burden in xenograft models. RKS262 is used in research on neuroblastoma and ovarian cancer [3].
Cat. No.: HY-159892
CAS No.: 1393644-68-2
Target:
Research Areas:
PD-1/PD-L1-IN-54 (Compound 6) is a moderately affinic PD-1/PD-L1 inhibitor (KD: PD-1, 55.8 μM; PD-L1, 46.4 μM; IC50: 88.6 μM). PD-1/PD-L1-IN-54 inhibits PD-1/PD-L1 interactions and shows anticancer activity by activating CD8 + T cells, upregulating PD-1 expression, and increasing secretion of IFN-γ and IL-2. PD-1/PD-L1-IN-54 inhibits cancer cell proliferation and promotes apoptosis. PD-1/PD-L1-IN-54 also regulates T cell immunity through the PI3K/Akt pathway correlated with PD-1/PD-L1 .
Cat. No.: HY-163962
CAS No.: 2451070-32-7
Target:
PROTACs Btk Bcr-Abl Toll-like Receptor (TLR) Fc Receptor (FcR) NOD-like Receptor (NLR) PERK p38 MAPK NF-κB TNF Receptor
Research Areas:
L18I is a Bruton's tyrosine kinase (BTK) PROTAC degrader that targets wild-type and BTK C481, and recruits the cereblon E3 ligase to mediate proteasomal degradation. L18I regulates the BCR, TLR, FcγR and NLRP3 inflammasome signaling pathways, inhibits the phosphorylation of PLCγ-2, ERK1/2 and p38, and reduces the levels of B cell activation markers CD25, CD69 and CD86. L18I downregulates the NF-κB, TNF and TLR signaling pathways, reduces the production of pro-inflammatory cytokines, and decreases immune cell infiltration and immune complex deposition. L18I inhibits the proliferation of BTK-expressing lymphoma cells, induces tumor regression in xenograft models, and exhibits synergistic activity when combined with inhibitors of SYK, PI3K or Lyn. L18I can be used in research related to lupus, diffuse alveolar hemorrhage and B-cell lymphoma [3] .
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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
