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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
140 Results for "
Jak/Stat pathway
" in MedChemExpress (MCE) Product Catalog:
Products (140)
140 Results for "Jak/Stat pathway" in MCE Product Catalog:
Cat. No.: HY-176876
CAS No.: 1198784-71-2
Research Areas:
Glucocorticoid receptor/IL-6-IN-1 (Compound 35) is a selective dual inhibitor targeting the glucocorticoid receptor (GR) and IL-6 signaling pathway (IC50 values of 120 nM and 59 nM, respectively). Glucocorticoid receptor/IL-6-IN-1 inhibits IL-6-induced JAK/STAT3 phosphorylation, blocking inflammatory cytokine transcription. Glucocorticoid receptor/IL-6-IN-1 is promising for research of inflammatory diseases like rheumatoid arthritis and asthma .
Cat. No.: HY-177515
CAS No.: 1356013-27-8
Research Areas:
IRAK4 modulator-2 (Compound 5) is a selective dual Interleukin-1 Receptor Associated Kinase 4 (IRAK4) and IRAK1 inhibitor with IC50 values of 0.005 μM and 0.97 μM, erespectively. IRAK4 modulator-2 blocks IRAK-mediated signaling pathways (e.g., JAK-STAT, NF-κB pathways), reduces the production of pro-inflammatory cytokines (e.g., IL-1, TNF), and exerts anti-inflammatory activity. IRAK4 modulator-2 is promising for research of autoimmune diseases and inflammatory diseases, such as rheumatoid arthritis, psoriasis, inflammatory bowel disease .
Cat. No.: HY-P99143
Target:
Research Areas:
Cat. No.: HY-189468
CAS No.: 3128784-74-4
PROTAC SHP2 degrader-1 is a potent SHP2 PROTAC degrader with a DC50 of 7.406 μM. PROTAC SHP2 degrader-1 recruits DCAF16 E3 ligase to induce ubiquitination and proteasomal degradation of SHP2, thereby inhibiting the RAS/MAPK and PI3K/AKT/mTOR signaling pathways while simultaneously inducing IFN-γ/JAK/STAT1, apoptosis, and cell cycle arrest. PROTAC SHP2 degrader-1 can be used for cancer research .
Cat. No.: HY-178500
CAS No.: 3052618-54-6
WCY-8-67 is an orally active and selective USP5 inhibitor, with an IC50 value of 1.33 μM. WCY-8-67 induces apoptosis and suppresses JAK/STAT3 and PI3K/AKT signaling pathways in vitro. WCY-8-67 inhibits proliferation of AE-positive AML cells, induces G1 phase arrest and differentiation of AML cells. WCY-8-67 demonstrates potent anti-leukemic efficacy in mice. WCY-8-67 can be used for the study of acute myeloid leukemia .
Cat. No.: HY-153858
CAS No.: 2470433-36-2
Research Areas:
PHI-501 is a dual inhibitor targeting RAF/DDR. PHI-501 exhibits significant anti-proliferative effects in melanoma cell lines and significantly inhibits the colony formation of drug-resistant cells. PHI-501 strongly inhibits ERK and AKT phosphorylation. PHI-501 downregulates the gene sets in drug-resistant cells of TNFA-NFKB, IL6-JAK-STAT3, and KRAS signaling pathways as well as the epithelial-mesenchymal transition (EMT) signaling pathways. PHI-501 demonstrates significant anti-tumor effects in the SK-MEL3DR xenograft model. PHI-501 can be used for research on the problem of drug resistance in melanoma .
Cat. No.: HY-178500A
WCY-8-67 TFA is an orally active and selective USP5 inhibitor, with an IC50 value of 1.33 μM. WCY-8-67 TFA induces apoptosis and suppresses JAK/STAT3 and PI3K/AKT signaling pathways. WCY-8-67 TFA inhibits proliferation of AE-positive AML cells, induces G1 phase arrest and differentiation of AML cells. WCY-8-67 TFA demonstrates potent anti-leukemic efficacy in mice. WCY-8-67 TFA can be used for the study of acute myeloid leukemia .
Cat. No.: HY-178716
CAS No.: 3093350-55-8
Target:
Research Areas:
PTPN2/1-IN-4 (Compound WS35) is an orally active, dual-functional inhibitor of PTPN1 and PTPN2 with IC50s of 12.8 and 5.8 nM for PTPN1 and PTPN2, respectively. PTPN2/1-IN-4 modulates the IFNγ-JAK-STAT signaling pathway and significantly augments CD8+ T-cell tumor infiltration. PTPN2/1-IN-4 has potent anticancer activity, robustly inhibiting tumor growth both as a monotherapy and in combination with an anti-PD-1 antibody in B16-OVA syngeneic mouse models .
Target:
Research Areas:
QL-1200186 is a selective, orally active, allosteric inhibitor targeting the tyrosine kinase TYK2 pseudokinase domain JH2 (IC50=0.06 nM, TYK2 JH2), with 164-fold selectivity over TYK1 JH2 (IC50=9.85 nM，TYK1 JH2). QL-1200186 first stabilizes the TYK2 JH2 conformation, inhibits the activity of the JH1 catalytic domain, and blocks the IFNα, IL-12/IL-23-mediated JAK-STAT signaling pathway. QL-1200186 can inhibit the production of Th1/Th17 cell-related cytokines (such as IFNγ, IL-23), reduce immune cell activation, and has no significant effect on JAK1/2/3 kinase activity. QL-1200186 can significantly improve skin inflammation in the Imiquimod (HY-B0180)-induced psoriasis mouse model and reduce the Psoriasis Area and Severity Index (PASI) score. QL-1200186 can be used in the study of autoimmune diseases such as psoriasis and systemic lupus erythematosus (SLE) .
Cat. No.: HY-N0732R
CAS No.: 37905-08-1
Cat. No.: HY-128854R
CAS No.: 792-74-5
Research Areas:
Dimethyl biphenyl-4,4'-dicarboxylate (Standard) is the analytical standard of Dimethyl biphenyl-4,4'-dicarboxylate (HY-128854). This product is intended for research and analytical applications. Dimethyl biphenyl-4,4'-dicarboxylate (Biphenyl dimethyl dicarboxylate) is a hepatoprotective agent. Dimethyl biphenyl-4,4'-dicarboxylate stimulates the Jak/Stat signaling pathway and induces the expression of IFN-α-stimulated genes, particularly 6-16 and ISG12. Dimethyl biphenyl-4,4'-dicarboxylate inhibits the replication of pregenomic RNA and HBeAg. Polymer micelles loaded with Dimethyl biphenyl-4,4'-dicarboxylate can serve as carriers for the compound. Dimethyl biphenyl-4,4'-dicarboxylate can be used as an auxiliary improving agent for chronic hepatitis. Dimethyl biphenyl-4,4'-dicarboxylate is applicable to research related to chronic hepatitis B .
Cat. No.: HY-128854S
CAS No.: 1219803-50-5
Cat. No.: HY-15244G
CAS No.: 1217486-61-7
Cat. No.: HY-15244R
CAS No.: 1217486-61-7
Synonyms: BYL-719 (Standard)
Target:
Research Areas:
Alpelisib (BYL-719) (Standard) is the analytical standard of Alpelisib (HY-15244). This product is intended for research and analytical applications. Alpelisib (BYL-719) is an orally active PI3Kα-selective inhibitor that blocks the conversion of PIP2 to PIP3, thereby inhibiting pathways including PI3K/AKT/mTOR, MAPK/ERK, Notch and JAK-STAT. Alpelisib also induces apoptosis, G0/G1 phase arrest and senescence; it significantly inhibits the proliferation, self-renewal, stemness and epithelial-mesenchymal transition (EMT) of tumor cells, reduces cancer stem cell populations and decreases the expression of stem cell markers. Alpelisib not only enhances the sensitivity to Eribulin (HY-13442) and exerts a synergistic effect with Paclitaxel (HY-B0015), but may also induce drug resistance by upregulating the SGK3/GSK3β/β-catenin signaling pathway. Alpelisib can be applied to research related to breast cancer, gastric cancer and lipomas associated with PTEN hamartoma tumor syndrome .
Cat. No.: HY-172581
CAS No.: 1862226-99-0
Clifutinib is an orally active and selective internal tandem duplication mutation of FMS-like tyrosine kinase 3 (FLT3-ITD) inhibitor with an IC50 value of 15.1 nM. Clifutinib exerts strong antiproliferative effects on FLT3-ITD acute myeloid leukemia (AML) cell lines (MV-4-11: IC50 = 1.5 nM; MOLM-13: IC50 = 1.4 nM). Clifutinib inhibits the activity of FLT3-ITD kinase and blocks the downstream RAS/MAPK, PI3K/AKT, and JAK/STAT5 signaling pathways of FLT3. Clifutinib induces apoptosis of acute myeloid leukemia (AML) cells with FLT3-ITD mutations. Clifutinib demonstrates significant antitumor efficacy in mice bearing MV-4-11 or MOLM-13 xenografts. Clifutinib is promising for research of relapsed/refractory FLT3-ITD-positive acute myeloid leukemia .
Cat. No.: HY-168894
Target:
Ferroptosis JAK STAT p38 MAPK AMPK GSK-3 Apoptosis HSP TNF Receptor
Research Areas:
Cardiovascular Disease Neurological Disease Metabolic Disease Cancer
CT-1 is a secreted protein belonging to the IL-6 cytokine family. Overexpression of CT-1 enhances cell proliferation, migration and angiogenesis via the ADMA/DDAH pathway. CT-1 inhibits the growth of triple-negative breast cancer cells by simultaneously inducing Ferroptosis in N2-type tumor-associated neutrophils and cancer cells. CT-1 activates the Jak/STAT-3, p42/p44 MAPK and AMPK pathways, and inhibits GSK-3β activity through phosphorylation to induce cardiomyocyte hypertrophy. CT-1 enhances the viability of cardiomyocytes and neurons, reduces cell Apoptosis, induces the expression of heat shock proteins (HSP) and BNP, and inhibits TNF levels. CT-1 exerts anti-tumor activity in mouse models of triple-negative breast cancer. CT-1 improves cognitive impairment in mice. CT-1 is applicable to the research of ischemic heart disease, triple-negative breast cancer, myocardial hypertrophy, Parkinson's disease, hypertensive heart disease, myocardial infarction, acute Chagas cardiomyopathy, high-fat diet-induced cognitive impairment and diabetes-related cognitive impairment .
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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
