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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
100 Results for "
overexpression
" in MedChemExpress (MCE) Product Catalog:
Products (100)
100 Results for "overexpression" in MCE Product Catalog:
179
179 Publications Verification
Mito-TEMPO is a mitochondria-targeted antioxidant. Mito-TEMPO induces mitophagy by activating the PINK1/Parkin pathway, inhibits NLRP3 inflammasome activation, restores mitochondrial membrane potential, and improves renal function and podocyte injury. Mito-TEMPO regulates Ca 2+ homeostasis, inhibits Bnip3 overexpression, shortens action potential duration, and exerts antiarrhythmic effects. Mito-TEMPO reverses premature senescence, reduces trabecular bone loss, and decreases cell apoptosis. Mito-TEMPO can be used in studies of chronic kidney disease, age-related cardiac dysfunction, postmenopausal osteoporosis, and ischemic stroke .
179
179 Publications Verification
Target:
Mitochondrial Metabolism PINK1/Parkin NOD-like Receptor (NLR) Autophagy Calcium Channel Apoptosis
Research Areas:
Cardiovascular Disease Neurological Disease Metabolic Disease Endocrinology
MitoTEMPO hydrate is a mitochondria-targeted antioxidant . MitoTEMPO hydrate induces mitophagy by activating the PINK1/Parkin pathway, inhibits NLRP3 inflammasome activation, restores mitochondrial membrane potential, and improves renal function and podocyte injury. MitoTEMPO hydrate regulates Ca 2+ homeostasis, inhibits Bnip3 overexpression, shortens action potential duration, and exerts antiarrhythmic effects. MitoTEMPO hydrate reverses premature senescence, reduces trabecular bone loss, and decreases cell apoptosis. MitoTEMPO hydrate can be used in studies of chronic kidney disease, age-related cardiac dysfunction, postmenopausal osteoporosis, and ischemic stroke .
6
6 Cited Publications
Cat. No.: HY-N0762
CAS No.: 31524-62-6
3
3 Cited Publications
Cat. No.: HY-163316
CAS No.: 3030697-87-8
Research Areas:
SIRT4-IN-1 is a selective and potent Sirtuin 4 (Sirt4) inhibitor with an IC50 of 16 μM for hSirt4. SIRT4-IN-1 also inhibits hSirt1, hSirt2, hSirt3, hSirt4 and hSirt6. SIRT4-IN-1 competes with acyl peptide substrate for Sirt4's acyl binding site, and is noncompetitive with NAD +. SIRT4-IN-1 increases glutamate dehydrogenase (GDH) activity and rescues pyruvate dehydrogenase (PDH) activity. SIRT4-IN-1 inhibits adipocyte differentiation and suppresses Sirt4 overexpression-induced increased differentiation. SIRT4-IN-1 can be used for the researches of cancer and metabolic disease .
2
2 Cited Publications
Target:
Research Areas:
NCGC00378430 is a potent SIX1/EYA2 interaction inhibitor. NCGC00378430 partially reverses transcriptional and metabolic profiles mediated by SIX1 overexpression and reverses SIX1-induced TGF-β signaling and epithelial-mesenchymal transition (EMT). NCGC00378430 inhibits SIX1-mediated breast cancer metastasis in a mouse model .
1
1 Cited Publications
Cat. No.: HY-NP159
1
1 Cited Publications
Target:
Opioid Receptor G Protein-coupled Receptor Kinase (GRK) Mas-related G-protein-coupled Receptor (MRGPR)
Research Areas:
CCG258747 is a selective GRK2 inhibitor (IC50 = 18 nM) with high selectivity over GRK1, GRK5, PKA, and ROCK1 (518, 83, > 5500, and > 550-fold, respectively). CCG258747 also blocks the internalization of the µ-opioid receptor (MOR). CCG258747 attenuates IgE mediated anaphylaxis by inhibiting GRK2 and FcεRI signaling pathway but activates mast cells via MRGPRX2 and MRGPRB2. CCG258747 can be used to study diseases related to overexpression of GRK2 (such as heart failure, opioid tolerance) .
1
1 Cited Publications
Cat. No.: HY-163121
CAS No.: 1096144-06-7
Research Areas:
PST3.1a is an orally active and brain-penetrant N-acetylglucosamine glycosyltransferase (MGAT5) inhibitor with a human IC50 of 2 µM. PST3.1a inhibits TGFβR and FAK signaling pathway activity. PST3.1a alters β1,6-GlcNAc N-glycans and microtubule/microfilament integrity, increases OLIG2 expression, and inhibits proliferation, migration, invasiveness, and clonogenic capacities of glioblastoma initiating cells. PST3.1a reduces invasive and proliferative capacity of glioblastoma initiating cells in orthotopic graft models, increases overall survival of orthotopic graft model mice. PST3.1a blunts MGAT5 overexpression, decreases renal fibrosis via collagen 1, collagen 4, and galectin 3 downregulation in a rat chronic kidney disease model. PST3.1a can be used for the research of glioblastoma multiforme and chronic kidney disease .
Target:
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Glycerol kinase, microorganism (GyK) acts as a NR4A1 inhibitor with enzymatic activity. It directly binds to and inhibits the transcription factor NR4A1, thereby negatively regulating hepatic gluconeogenesis and reducing blood glucose levels. Glycerol kinase, microorganism positively regulates UCP1 expression via partial dependence on the β-adrenergic receptor-cAMP-CREB pathway, promotes browning of white adipose tissue and thermogenesis, and further modulates intracellular fatty acid composition and energy metabolism. In diabetic mouse models, overexpression of Glycerol kinase effectively antagonizes NR4A1-induced hyperglycemia, demonstrating potential for improving glucose homeostasis. Glycerol kinase, microorganism can be used for studies on diabetes and obesity .
Cat. No.: HY-B0815S
CAS No.: 285138-81-0
Cat. No.: HY-W704574
CAS No.: 77102-28-4
Research Areas:
Mergetpa is a reversible Arg-carboxypeptidase inhibitor with high affinity. Mergetpa reduces B1R. Mergetpa blocks the overexpression of IL-1β protein and mRNA in glucose-fed rats. Mergetpa significantly increases the expression of IL-1β protein in the renal cortex. Mergetpa is used to block the conversion of kinins and B2 receptor antagonists into metabolites lacking the C-terminal arginine. Mergetpa inhibits the time-dependent enhancement of the response of isolated rabbit aorta to bradykinin. Mergetpa preserves the chemotactic activity of full-length SDF-1α on cells. Mergetpa reverses hyperglycemia, excessive weight gain, elevated levels of oxidative stress markers and overexpression of inflammatory markers in glucose-fed rats .
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 .
ASR-490 reduces the viability of HCT116 and SW620 cells by downregulating Notch1 signaling. ASR-490 overcomes Notch1 overexpression and inhibits the growth of HCT/Notch1 transfectants. ASR-490 inhibits the tumor growth in control (pCMV/HCT116) and Notch1/HCT116 in xenotransplanted mice .
Cat. No.: HY-N6663
CAS No.: 13466-78-9
Category:
Other Monoterpenes other families Terpenoids Plants Disease Research Fields Inflammation/Immunology
Target:
Cat. No.: HY-172825
KL4-219A is a selective covalent oncogenic transcription factor MYC degrader. KL4-219A potently and durably degrades MYC in cancer cells. KL4-219A binds covalently to MYC at C203, leading to the destabilization of MYC and subsequent proteasome-dependent degradation. KL4-219A is promising for research of cancers driven by MYC overexpression .
Cat. No.: HY-P4190
CAS No.: 163973-98-6
Target:
Research Areas:
Cat. No.: HY-P3136
CAS No.: 25849-90-5
Synonyms: TRV120055
Target:
Research Areas:
Cat. No.: HY-159904
Target:
Research Areas:
ChAT IN-1 is a selective Choline Acetyltransferase (ChAT) inhibitor. It can be used to study mechanisms related to the overexpression of non-neuronal ChAT in cancers (e.g., colorectal and lung cancers) and Alzheimer’s disease (AD) .
Cat. No.: HY-W342380
CAS No.: 5463-64-9
Synonyms: NSC 5067
Target:
Research Areas:
SPI-05 (NSC 5067) is a non-competitive SUMO-specific proteases (SENP1/2) inhibitor (IC50=60 μM). SPI-05 is promising for research of cancers, such as prostate cancer and hypoxia-driven solid tumors with SENP1 overexpression .
Cat. No.: HY-P11020
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Research Areas:
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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
