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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
935 Results for "
Normal
" in MedChemExpress (MCE) Product Catalog:
Products (935)
935 Results for "Normal" in MCE Product Catalog:
Cat. No.: HY-113277R
CAS No.: 3058-01-3
Cat. No.: HY-167825
CAS No.: 24506-68-1
Cat. No.: HY-174460
Target:
Research Areas:
pCR8 is a CR8 prodrug and anticancer agent responsive to H2O2. pCR8 achieves selective release of CR8 via boronate ester oxidation mediated by elevated hydrogen peroxide levels at tumor sites, self-assembles into nanoparticles, and degrades cell cycle-related proteins. A synergistic effect is produced when pCR8 is used in combination with immune checkpoint inhibitors. pCR8 can be used for the research of triple-negative breast cancer .
Cat. No.: HY-183308
Antifungal agent-161 (Compound 7) is an Antifungal agent. Antifungal agent-161 potently inhibits Candida albicans ATCC 36082 (with a MIC of 1.32 μM) and Candida glabrata ATCC 2001 (with a MIC of 1.66 μM). Antifungal agent-161 reduces fungal loads in infected mice and eliminates Candida albicans and Candida glabrata infections. Antifungal agent-161 can be used for the research of candidiasis .
Cat. No.: HY-D3188
CAS No.: 2730023-28-4
Cat. No.: HY-P11590
Cat. No.: HY-P11797
Target:
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Cat. No.: HY-161995
FGFR1/VEGFR2-IN-2 (compound 6l) is a VEGFR2/FGFR1 dual inhibitor. The IC50 values for VEGFR2 and FGFR1 are 0.025 µM and 0.026 µM respectively, and for EGFR and PDGFR-β, the IC50 values are 0.106 µM and 0.077 µM. FGFR1/VEGFR2-IN-2 showes significant anti-cancer activity (GI=60.38%) on NCI-60 cell line, with an IC50 of 8.51 µM in T-47D cell line and anti-migration. FGFR1/VEGFR2-IN-2 acts to arrest cells in the G1 phase and promote apoptosis and necrosis; the IC50 for MCF-7 cell line exceeds 100 µM, and the IC50 for MDA-MB-231 is 69.17 µM, non-toxic to normal cells .
Cat. No.: HY-178032
Research Areas:
PARP1-IN-44, an Olaparib (HY-10162) derivative, is an orally active PARP1 inhibitor (IC50 = 0.6 nM), and also inhibits PARP2 (IC50 = 1.0 nM) and PARP7 (IC50 = 7.5 nM). PARP1-IN-44 has selective antiproliferative activity against BRCA-deficient cancer cells with minimal toxicity to normal cells. PARP1-IN-44 induces G2/M phase arrest, promotes apoptosis, elevates ROS levels, disrupts mitochondrial membrane potential. PARP1-IN-44 suppresses PARylation while increasing γH2AX accumulation. PARP1-IN-44 activates the cGAS-STING pathway, upregulating IFN-β and CXCL10 expression. PARP1-IN-44 enhancing CD8+ T cell infiltration in a CT26 tumor mouse model, demonstrating robust in vivo antitumor efficacy .
Cat. No.: HY-182354
CAS No.: 861877-12-5
VEGFR2-IN-84 is an orally active, multi-targeted tyrosine kinase inhibitor based on a naphthalene ring scaffold. VEGFR2-IN-84 inhibits VEGFR2 with sub-nanomolar affinity and broadly targets kinases including Kit, FGFR, PDGFR, and Ret. By competitively binding to the ATP-binding pocket, VEGFR2-IN-84 blocks the phosphorylation of VEGFR2 and its downstream AKT/ERK signaling pathway, thereby significantly inhibiting endothelial cell proliferation, migration, and tumor angiogenesis. VEGFR2-IN-84 exhibits broad-spectrum antiproliferative activity against various solid tumors such as liver cancer, lung cancer, and renal cancer, shows weak toxicity to normal cells, and has superior potency to Lenvatinib (HY-10981). VEGFR2-IN-84 possesses favorable pharmacokinetic properties and high safety (LD50>2000 mg/kg), and can be used in related studies of various malignant tumors .
Cat. No.: HY-182745
VEGFR-2-IN-85 is a strong VEGFR-2 inhibitor, with an IC50 value of 0.23 μM. VEGFR-2-IN-85 exhibits potent cytotoxic activity against multiple cancer cell lines with minimal toxicity toward normal cells. VEGFR-2-IN-85 also impairs cancer cell migration, likely through modulation of the VEGFR-2/p-Akt pathway. VEGFR-2-IN-85 can induce apoptosis through modulation of Caspase-3, Bax and Bcl-2. VEGFR-2-IN-85 arrests cell cycle at the G2/M phase and has anti-angiogenic activity. VEGFR-2-IN-85 is a targeted radiosensitizer enhancing radiation-induced cytotoxicity. VEGFR-2-IN-85 can be used for research on cancers such as non-small cell lung cancer, breast cancer, and liver cancer .
Cat. No.: HY-183355
Research Areas:
KRAS G12D-IN-37 is a KRAS G12D inhibitor. KRAS G12D-IN-37 shows antiproliferative activity against KRAS G12D mutant tumor cells and minimal cytotoxicity toward normal cells. KRAS G12D-IN-37 binds stably to KRAS G12D via hydrogen bond interactions with residues His 95, Arg 68, and Asp 12, and inhibits downstream ERK/AKT signaling pathways. KRAS G12D-IN-37 elevates ROS levels, induces apoptosis, disrupts mitochondrial membrane potential. KRAS G12D-IN-37 downregulates the level of anti-apoptotic protein Bcl-2, and upregulates the levels of pro-apoptotic proteins Bax and caspase 3. KRAS G12D-IN-37 can be used for the research of cancer, such as gastric adenocarcinoma and colorectal cancer .
Cat. No.: HY-B0366AR
CAS No.: 969-33-5
Synonyms: Cyproheptadine HCl (Standard)
Target:
Reference Standards p38 MAPK Checkpoint Kinase (Chk) Histamine Receptor 5-HT Receptor CDK PARP Apoptosis
Research Areas:
Cyproheptadine hydrochloride (Standard) (Cyproheptadine HCl (Standard)) is the analytical standard of Cyproheptadine hydrochloride (HY-B0366A). This product is intended for research and analytical applications. Cyproheptadine hydrochloride (Cyproheptadine HCl) acts as a p38 MAP kinase activator, CHK2 activator, histamine H1 receptor inhibitor and serotonin receptor inhibitor. Cyproheptadine hydrochloride mediates cell cycle arrest via G1 phase arrest, G1/S transition arrest, G0/G1 phase arrest, reduced expression of cyclins D1/D2/D3, upregulated expression of HBP1, p16, p21, p27, and decreased phosphorylation of retinoblastoma protein. Cyproheptadine hydrochloride induces Apoptosis by increasing PARP and cleaved PARP, as well as activating the mitochondrial caspase pathway. Cyproheptadine hydrochloride inhibits tumor growth with extremely low toxicity to normal cells. Cyproheptadine hydrochloride can be used in research related to hepatocellular carcinoma, multiple myeloma and acute myeloid leukemia .
Cat. No.: HY-B0377A
CAS No.: 125193-62-6
Synonyms: MK-208 hydrochloride
Research Areas:
Famotidine hydrochloride (MK-208 hydrochloride) is an orally active and highly selective histamine H2 receptor antagonist. It inhibits gastric acid secretion by blocking the Gs signaling pathway, and regulates intracellular cAMP and ERK pathways. Famotidine hydrochloride inhibits TLR3-mediated inflammatory pathways, and reduces the expression of various inflammatory mediators and interferon-related genes. Famotidine hydrochloride scavenges DPPH and nitric oxide free radicals, alleviates oxidative stress damage in gastric tissue, inhibits proMMP-9, improves vascular endothelial permeability, and restores the normal physiological functions of neutrophils and eosinophils. Famotidine hydrochloride crosses intestinal epithelial cells via facilitated diffusion and passive diffusion, blocks paracellular cation transport, and increases intestinal transepithelial electrical resistance. Famotidine hydrochloride reduces serum levels of transaminases and alkaline phosphatase, exerts analgesic effects and gastric protective effects simultaneously. Famotidine hydrochloride can be used in studies related to COVID-19, liver injury and acute gastric ulcer .
Target:
Reference Standards p38 MAPK Checkpoint Kinase (Chk) Histamine Receptor 5-HT Receptor CDK PARP Apoptosis
Research Areas:
Cyproheptadine (Standard) is the analytical standard of Cyproheptadine (HY-B1622). This product is intended for research and analytical applications. Cyproheptadine acts as a p38 MAP kinase activator, CHK2 activator, histamine H1 receptor inhibitor and serotonin receptor inhibitor. Cyproheptadine mediates cell cycle arrest via G1 phase arrest, G1/S transition arrest, G0/G1 phase arrest, reduced expression of cyclins D1/D2/D3, upregulated expression of HBP1, p16, p21, p27, and decreased phosphorylation of retinoblastoma protein. Cyproheptadine induces Apoptosis by increasing PARP and cleaved PARP, as well as activating the mitochondrial caspase pathway. Cyproheptadine inhibits tumor growth with extremely low toxicity to normal cells. Cyproheptadine can be used in research related to hepatocellular carcinoma, multiple myeloma and acute myeloid leukemia .
Cat. No.: HY-B1622S
CAS No.: 2712455-05-3
Target:
Isotope-Labeled Compounds p38 MAPK Checkpoint Kinase (Chk) Histamine Receptor 5-HT Receptor CDK PARP Apoptosis
Research Areas:
Cyproheptadine-d3 is the d3-labeled Cyproheptadine (HY-B1622). Cyproheptadine acts as a p38 MAP kinase activator, CHK2 activator, histamine H1 receptor inhibitor and serotonin receptor inhibitor. Cyproheptadine mediates cell cycle arrest via G1 phase arrest, G1/S transition arrest, G0/G1 phase arrest, reduced expression of cyclins D1/D2/D3, upregulated expression of HBP1, p16, p21, p27, and decreased phosphorylation of retinoblastoma protein. Cyproheptadine induces Apoptosis by increasing PARP and cleaved PARP, as well as activating the mitochondrial caspase pathway. Cyproheptadine inhibits tumor growth with extremely low toxicity to normal cells. Cyproheptadine can be used in research related to hepatocellular carcinoma, multiple myeloma and acute myeloid leukemia .
Cat. No.: HY-P10862
Target:
IC50 values of 11.9, 12.5, 35.7, 206 and 136 nM, respectively. AH-D peptide reduces the viral load in the brain, suppresses inflammation, protects neurons, and does not damage the blood brain barrier. AH-D peptide restores antitumor immunity by decreasing circulating PD-L1 + exosomes, reducing intratumoral immunosuppressive cells (regulatory T cells, myeloid-derived suppressor cells), and enhancing T cell function. AH-D peptide inhibits membrane-enveloped viruses and cancer cell metastasis in vivo. AH-D peptide exhibits no immunogenicity and has negligible effects on normal tissues. AH-D peptide can be used for research in Zika virus and other mosquito-borne viruses, cancer immunotherapy and metastasis .
Cat. No.: HY-L079
4,333 compounds
Blood cancers, also called hematologic cancers, occur when abnormal blood cells start growing out of control, interrupting the function of normal blood cells, which fight off infection and produce new blood cells. Most blood cancers start in the bone marrow, which is where blood is produced. There are three main types of blood cancers: leukemia, lymphoma and myeloma, which afflict millions of children and adults every year, and are often deadly.
Some common blood cancer treatments include stem cell transplantation, chemotherapy, radiation therapy, targeted therapy, immunotherapy or a combination thereof. As we begin to understand the key signaling pathways and molecular drivers of malignant transformation in haematological disorders, new treatment strategies will continue to be developed.
MCE offers a unique collection of 4,333 compounds with identified and potential anti-blood cancer activity. These compounds target blood cancer’s major targets and signaling pathways. MCE anti-blood cancer compound library is a useful tool for anti-blood cancer drugs screening and other related research.
Cat. No.: HY-160952
CAS No.: 1256639-86-7
Synonyms: CPX 351; Cytarabine-daunorubicin
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Research Areas:
Cytarabine-daunorubicin (CPX 351) is a Liposomal formulation prepared from Cytarabine (HY-13605) and Daunorubicin (HY-13062A) at a fixed synergistic molar ratio of 5:1. Cytarabine-daunorubicin improves secondary acute myeloid leukemia. Cytarabine-daunorubicin can be used in research related to secondary acute myeloid leukemia, high-risk myelodysplastic syndrome, and chronic myelomonocytic leukemia .
Cat. No.: HY-172937
CAS No.: 3070968-56-5
Research Areas:
ERα degrader 13 is an orally active, methylene blue-Raloxifene (HY-13738) conjugated photoactivatable ERα degrader with a Kd value of 27.1 nM. Upon irradiation at 660 nm, ERα degrader 13 generates ROS and heat near the ligand-binding domain of ERα, triggering oxidation, residue unfolding, and ERα degradation via the ubiquitin-proteasome system. ERα degrader 13 inhibits cancer cell proliferation and induces tumor regression in breast cancer xenograft models. ERα degrader 13 can be used in breast 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
