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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
1287 Results for "
differentiated
" in MedChemExpress (MCE) Product Catalog:
Products (1287)
1287 Results for "differentiated" in MCE Product Catalog:
Cat. No.: HY-N0515R
CAS No.: 945619-74-9
Cat. No.: HY-N1970R
CAS No.: 31721-94-5
Category:
other families Flavonoids Phenols Polyphenols Plants Isoflavones
Target:
Cat. No.: HY-W014937S
CAS No.: 93496-64-1
Synonyms: 4HBP-d4
4-Hydroxybenzophenone-d4 (4HBP-d4) is the deuterated-labeled 4-Hydroxybenzophenone (HY-W014937). 4‑Hydroxybenzophenone (4HBP) is a major metabolite of Benzophenone (HY-Y0546) and is orally active. 4-Hydroxybenzophenone triggers endoplasmic reticulum stress and activates the PERK-eIF2α-ATF4-CHOP and IRE1α-XBP1s pathways, and inhibits IκB translation. 4-Hydroxybenzophenone induces endoplasmic reticulum stress, unfolded protein response activation, protein homeostasis imbalance, protein aggregation, oxidative stress, ROS accumulation, mitochondrial membrane potential decrease, ATP depletion, and cytotoxicity. 4-Hydroxybenzophenone induces neural stem cell apoptosis (apoptosis) and affects neuronal differentiation. 4-Hydroxybenzophenone promotes malignant proliferation of hepatocellular carcinoma cells and xenograft tumor growth in nude mice. 4-Hydroxybenzophenone can be used in research related to neurodevelopmental toxicity and hepatocellular carcinoma .
Cat. No.: HY-W014937S1
CAS No.: 76478-47-2
Synonyms: 4HBP-d5
4-Hydroxybenzophenone-d5 (4HBP-d5) is the deuterated-labeled 4-Hydroxybenzophenone (HY-W014937). 4‑Hydroxybenzophenone (4HBP) is a major metabolite of Benzophenone (HY-Y0546) and is orally active. 4-Hydroxybenzophenone triggers endoplasmic reticulum stress and activates the PERK-eIF2α-ATF4-CHOP and IRE1α-XBP1s pathways, and inhibits IκB translation. 4-Hydroxybenzophenone induces endoplasmic reticulum stress, unfolded protein response activation, protein homeostasis imbalance, protein aggregation, oxidative stress, ROS accumulation, mitochondrial membrane potential decrease, ATP depletion, and cytotoxicity. 4-Hydroxybenzophenone induces neural stem cell apoptosis (apoptosis) and affects neuronal differentiation. 4-Hydroxybenzophenone promotes malignant proliferation of hepatocellular carcinoma cells and xenograft tumor growth in nude mice. 4-Hydroxybenzophenone can be used in research related to neurodevelopmental toxicity and hepatocellular carcinoma .
Cat. No.: HY-W509797
CAS No.: 21618-92-8
Target:
Drug Metabolite TNF Receptor IKK NF-κB Autophagy NOD-like Receptor (NLR) NADPH Oxidase Keap1-Nrf2
Research Areas:
5-(3',4'-Dihydroxyphenyl)-γ-valerolactone is an intestinal microbiota metabolite of (-)-Epicatechin (HY-N0001). 5-(3',4'-Dihydroxyphenyl)-γ-valerolactone downregulates TNF-α-stimulated phosphorylation of IKK and IκBα, inhibits the transcriptional activation of NF-κB, and suppresses the expression of adhesion molecules and chemokines. 5-(3',4'-Dihydroxyphenyl)-γ-valerolactone promotes autophagy, alleviates oxidative stress, maintains osteoblast differentiation, induces G1 phase arrest, inhibits adipogenesis, and scavenges ABTS free radicals. 5-(3',4'-Dihydroxyphenyl)-γ-valerolactone inhibits the adhesion of uropathogenic Escherichia coli to bladder epithelial cells; when used in combination with Curcumin (HY-N0005), it downregulates the NLRP3 and NOX2/Nrf2 signaling pathways, thereby reducing microglial activation. 5-(3',4'-Dihydroxyphenyl)-γ-valerolactone can be used in research related to diabetes, atherosclerosis, osteoporosis, obesity, neurodegenerative diseases involving microglial activation, and urinary tract infections .
Cat. No.: HY-171906A
Synonyms: 1-Arachidonoyl-sn-glycerol 3-phosphate sodium; 1-Arachidonoyl LPA sodium; LPA (20:4) sodium
Target:
Research Areas:
1-Arachidonoyl-2-hydroxy-sn-glycero-3-PA (sodium) (1-Arachidonoyl-sn-glycerol 3-phosphate (sodium)) is a phospholipid with arachifonic acid at the sn-1 position. 1-Arachidonoyl-2-hydroxy-sn-glycero-3-PA (sodium) binds to the LPA2/EDG4 receptor (EC50 of 10 nM). 1-Arachidonoyl-2-hydroxy-sn-glycero-3-PA (sodium) can be found in rat brain as 37% of the arachidoinic acid-containing lysophosphatidic acid species. 1-Arachidonoyl-2-hydroxy-sn-glycero-3-PA (sodium) is the precursor to 1-arachidonoyl glycerol. 1-Arachidonoyl-2-hydroxy-sn-glycero-3-PA (sodium) can prevent TNF-α and IL-6 secretion in wild type LPS-stimulated dendritic cells. 1-Arachidonoyl-2-hydroxy-sn-glycero-3-PA (sodium) reduces differentiation of HT-29 colon carcinoma cells into goblet cells when sodium butyrate is present .
Cat. No.: HY-B0110S
CAS No.: 1542211-40-4
Synonyms: SHB 331-d6; WL 70-d6
Gestodene-d6 (SHB 331-d6; WL 70-d6) is the deuterated-labeled Gestodene (HY-B0110). Gestodene is an orally active synthetic progestogen compound of the 19-nortestosterone class. Gestodene binds with high affinity to the progesterone receptor, inhibits 5α-reductase, binds to androgen and aldosterone receptors, and inactivates CYP3A. Gestodene acts as a positive allosteric modulator of PAR1, enhances PAR1-mediated signaling pathways, and is capable of increasing the activation potency of PAR1-AP toward PAR1, thereby promoting ERK1/2 phosphorylation, receptor internalization, cell morphological changes, and human platelet aggregation. Gestodene and its A-ring reduced metabolites promote the proliferation, differentiation, and mineralization of neonatal rat osteoblasts. Gestodene itself has no binding capacity for estrogen receptors, and this osteogenic activity depends on intracellular metabolism to generate A-ring reduced products with estrogen-like agonistic activity. Gestodene is useful for research on diseases related to progesterone secretion and diseases related to thrombosis .
Cat. No.: HY-N2593R
CAS No.: 32507-66-7
Cat. No.: HY-W028393R
CAS No.: 392-12-1
Category:
Cat. No.: HY-W753897
Synonyms: SHB 331-d7; WL 70-d7
Gestodene-d7 (SHB 331-d7; WL 70-d7) is the deuterated-labeled Gestodene (HY-B0110). Gestodene is an orally active synthetic progestogen compound of the 19-nortestosterone class. Gestodene binds with high affinity to the progesterone receptor, inhibits 5α-reductase, binds to androgen and aldosterone receptors, and inactivates CYP3A. Gestodene acts as a positive allosteric modulator of PAR1, enhances PAR1-mediated signaling pathways, and is capable of increasing the activation potency of PAR1-AP toward PAR1, thereby promoting ERK1/2 phosphorylation, receptor internalization, cell morphological changes, and human platelet aggregation. Gestodene and its A-ring reduced metabolites promote the proliferation, differentiation, and mineralization of neonatal rat osteoblasts. Gestodene itself has no binding capacity for estrogen receptors, and this osteogenic activity depends on intracellular metabolism to generate A-ring reduced products with estrogen-like agonistic activity. Gestodene is useful for research on diseases related to progesterone secretion and diseases related to thrombosis .
Cat. No.: HY-L228
146 compounds
Lipids are important energy storage substances in the human body. They are involved in the regulation of cell structure and function, as well as signaling pathways and gene expression. Abnormal lipid levels in tissues or their dysregulation can lead to various diseases. These include obesity, type 2 diabetes, non-alcoholic fatty liver disease, neurodegenerative diseases, infections, and cancer. Therefore, maintaining normal levels of lipid metabolism is critical to overall health.
One of the key features of cancer is aberrant lipid metabolism. This includes alterations in lipid uptake, lipid desaturation, neolipogenesis, lipid droplets, and fatty acid oxidation in cancer cells. These changes all contribute to cellular survival in an ever-changing microenvironment. They do this by modulating feed-forward oncogenic signals and key oncogenic functions. Additionally, they affect oxidative stress, other types of stress, immune responses, and intercellular communication. Alterations in lipid metabolism have a strong impact on the properties of cancer stem cells. This includes aspects such as self-renewal, differentiation, invasion, metastasis, drug sensitivity, and resistance. Furthermore, these alterations also modulate T cell responses.
MCE can offer 146 metabolites of lipid metabolism pathways, which can be used for drug screening in cancer, immune-based diseases, metabolic diseases, and other diseases.
Cat. No.: HY-L135
3,540 compounds
With the progress of modern cancer therapy, the life of cancer patients has been extended. However, after initial treatment and recovery, the development of secondary tumors often leads to cancer recurrence. Cancer stem cells are a small number of cells that tumor growth and reproduction depend on.
Cancer stem cells have strong self-renewal ability, which is the direct cause of tumor occurrence. In addition, cancer stem cells also have the ability to differentiate into different cell types, playing a crucial role in tumor metastasis and development. Chemotherapy and radiotherapy induced DNA damage and apoptosis are common cancer treatments. However, cancer stem cells can effectively protect cancer cells from apoptosis by activating DNA repair ability. Cancer stem cells are regarded as the key "seed" of tumor occurrence, development, metastasis and recurrence. Since its first discovery in leukemia in 1994, cancer stem cells have been considered a promising therapeutic target for cancer treatment.
MCE supplies a unique collection of 3,540 compounds targeting key proteins in cancer stem cells. MCE Cancer Stem Cells Compound Library is a useful tool for cancer stem cells related research and anti-cancer drug development.
Cat. No.: HY-L018
458 compounds
The transforming growth factor beta (TGF-β) signaling pathway is involved in many cellular processes in both the adult organism and the developing embryo including cell growth, cell differentiation, apoptosis, cellular homeostasis and other cellular functions. The TGF-β superfamily comprises TGF-βs, bone morphogenetic proteins (BMPs), activins and related proteins. Signaling begins with the binding of a TGF beta superfamily ligand to a TGF beta type II receptor. The type II receptor is a serine/threonine receptor kinase, which catalyzes the phosphorylation of the Type I receptor. The type I receptor then phosphorylates receptor-regulated SMADs (R-SMADs) which can now bind the coSMAD (e.g. SMAD4). R-SMAD/coSMAD complexes accumulate in the nucleus where they act as transcription factors and participate in the regulation of target gene expression. Deregulation of TGF-β signaling contributes to developmental defects and human diseases, including cancers, some bone diseases, chronic kidney disease, etc.
MCE designs a unique collection of 458 TGF-beta/Smad signaling pathway compounds. TGF-beta/Smad Compound Library acts as a useful tool for TGF-beta/Smad-related drug screening and disease research.
Target:
Research Areas:
Xylamidine is a peripheral 5-HT receptor antagonist used to investigate possible peripheral appetite suppressant effects of 5-hydroxytryptophan (5-HTP) and fenfluramine. In a 1-hour food intake test, xylamidine attenuated the decrease in food intake induced by 5-HT and 5-HTP, but had no effect on fenfluramine, suggesting that the appetite suppressant effect of 5-HTP is mediated in part through peripheral 5-HT receptors. Microstructural analysis revealed that 5-HTP and fenfluramine induced a decrease in food intake rate and a reduction in feeding batch size. Xylamidine reversed the effects of 5-HTP on food intake rate and induced a slight increase in feeding batch size itself, thus, the peripheral effect of 5-HTP appears to be to slow food intake rate. No effect of xylamidine on fenfluramine-induced changes in feeding was observed. The results suggest that the appetite suppressant effects of 5-HTP and fenfluramine are differentiated based on the peripheral effects of 5-HTP. The peripheral effects of 5-HTP are distinct from the previously reported 5-HT-induced decreases in feeding batch size and duration. Possible mechanisms underlying the differences in peripheral effects of 5-HT and 5-HTP are discussed.
Cat. No.: HY-117947
CAS No.: 1809336-19-3
Target:
Research Areas:
(R)-OR-S1 is an isomer of OR-S1. The dual ZH1/2 inhibitors OR-S1 and OR-S2 exhibit strong inhibitory activity against both EZH1 and EZH2. OR-S1 and OR-S2 are highly selective methyltransferase inhibitors against EZH1 and EZH2, and they have very similar molecular features. Therefore, we investigated the effect of OR-S1 on acute myeloid leukemia (AML). We found that OR-S1 was able to induce cell differentiation and apoptosis in AML cells. These findings encouraged us to investigate whether functional LT-HSCs could survive PRC2-targeted therapy with OR-S1 or OR-S1 combined with cytarabine. The results showed that OR-S1 did not cause significant myelosuppression, and BM cells treated with the combination therapy were able to undergo normal hematopoiesis even 4 months after treatment. Therefore, temporary inhibition of EZH1 and EZH2 is clinically tolerable, making this combination therapy suitable for AML patients. AML is generally believed to originate from myeloid progenitor cells that inherit a large number of biological properties.
Research Areas:
U7D-1 is a USP7 PROTAC degrader that induces selective proteasomal degradation of USP7. U7D-1 destabilizes and downregulates the expression of variant PRC1 complex subunits PCGF1, RING1A and PCGF6, and also slightly reduces the protein level of KDM2B. U7D-1 decreases cell viability, arrests neuroblastoma cells at the G0/G1 cell cycle phase, and downregulates the expression of target genes of PAX3::FOXO1 in FP-RMS cells. U7D-1 increases the level of cleaved PARP in FP-RMS cells, induces cell apoptosis, and upregulates the expression of muscle differentiation markers MYH1 and MYF5. U7D-1 inhibits the growth and proliferation of p53 wild-type and mutant cancer cells, and regulates the apoptosis pathway and E2F pathway. U7D-1 is applicable to studies on neuroblastoma, fusion-positive rhabdomyosarcoma, p53-mutant cancers and cancer-related research .
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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
