Scientific Reviews
Product Guides
Blogs
Topics
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
378 Results for "
AML
" in MedChemExpress (MCE) Product Catalog:
Products (378)
378 Results for "AML" in MCE Product Catalog:
Cat. No.: HY-P990905
CAS No.: 2871775-98-1
Synonyms: SAR-443579
Target:
Research Areas:
Cat. No.: HY-P991425
Target:
Research Areas:
Cat. No.: HY-P99916
CAS No.: 2449199-61-3
Synonyms: AMG-427
Target:
Research Areas:
Cat. No.: HY-115590
CAS No.: 1902983-63-4
JP-11646 is a pan-PIM inhibitor with increased potency against PIM2 (IC50 = 0.5 nM). JP11646 is freely reversible and ATP non-competitive. JP-11646 results in a decrease of PIM1, 2, and 3 mRNA. JP-11646 can effectively inhibit cell viability in small cell lung cancer (SCLC) and large cell neuroendocrine carcinomas of the lung (LCNEC). JP-11646 can cause a decrease in p-4EBP-1 protein, increasing the cleavage of caspases while decreasing caspase-3. JP-11646 induces apoptosis or necroptosis in cells. JP-11646 leads to reductions in MYC paralogs. JP-11646 can be used for the study of SCLC, LCNEC, human acute leukemia (AML), multiple myeloma (MM), and triple-negative breast cancer (TNBC) .
Synonyms: BRD5846
Target:
Research Areas:
BAY-888 is a selective CK1α/CSNK1A1 (casein kinase 1α) ATP-competitive inhibitor (IC50: 4 nM@10 μM ATP; 63 nM@1 mM ATP). BAY-888 blocks the negative regulation of p53 and other signaling pathways by CK1α, induces apoptosis and inhibits proliferation of tumor cells. BAY-888 has shown inhibitory efficacy against cancers such as acute myeloid leukemia (AML) in PRISM barcoded cell line screening and can mimic the effects of shRNA-mediated CK1α knockdown. BAY-888 is primarily used for the development of anticancer drugs for p53 wild-type tumors and for the study of the mechanisms of CK1α-related signaling pathways .
Cat. No.: HY-175282A
CAS No.: 2748800-07-7
(2S,3R,4S)-ASX-173 is the (2S,3R,4S)-enantiomer of ASX-173 (HY-175282). ASX-173 is an orally active inhibitor of asparagine synthetase (ASNS) (IC50 = 0.113 μM, Ki = 0.4 nM). ASX-173 enhances the anticancer activity of L-asparaginase (ASNase) (HY-P1923). ASX-173 disrupts nucleotide synthesis and induces leukemia cell cycle arrest, apoptosis and autophagy in leukemia cells in combination with ASNase. ASX-173 slows the growth of OCI-AML2 xenografts in combination with ASNase. ASX-173 is indicated for the study of acute lymphoblastic leukemia, acute myeloid leukemia, colorectal cancer, and other cancers .
Cat. No.: HY-178020
CAS No.: 3020729-11-4
FLT3-IN-34 is a FLT3 inhibitor, with an IC50 value of 1.4 nM. FLT3-IN-34 blocks the phosphorylation of FLT3 and its downstream signaling molecules AKT and ERK1/2. FLT3-IN-34 induces concentration-dependent G0/G1 phase arrest and mild apoptosis in FLT3-ITD-positive MV4-11 cells. FLT3-IN-34 shows potent anti-proliferative activity against FLT3-ITD-positive MV4-11 cells (IC50 = 14.95 nM) and MOLM-13 (IC50 = 18.5 nM). FLT3-IN-34 can be used for the study of FLT3-positive acute myeloid leukemia (AML) .
Cat. No.: HY-179272
CAS No.: 3037071-29-4
Wee1/HDAC-IN-1 is a dual Wee1/HDAC inhibitor with an IC50 of 1.2 nM for Wee1 and IC50 values of 196 nM for HDAC1, 156 nM for HDAC3, and 55 nM for HDAC6. Wee1/HDAC-IN-1 exhibits strong antiproliferative activity against MV4-11 cells with an IC50 of 0.076 μM. Wee1/HDAC-IN-1 selectively binds to Wee1 and HDACs. Wee1/HDAC-IN-1 interferes with DNA damage repair pathways and induces apoptosis in MV4-11 cells. Wee1/HDAC-IN-1 Wee1/HDAC-IN-1 can be used for the research of acute myeloid leukemia (AML) .
Cat. No.: HY-182356
CAS No.: 3125953-25-2
Research Areas:
MTHFD1/2-IN-1 is an orally active dual MTHFD1/MTHFD2 inhibitor, with IC50 values of 0.26 μM and 0.031 μM against human MTHFD1 and MTHFD2, respectively. MTHFD1/2-IN-1 blocks one-carbon metabolism by inhibiting the dehydrogenase activity of MTHFD1 as well as the dehydrogenase and cyclohydrolase activities of MTHFD2, thereby disrupting nucleotide biosynthesis and redox homeostasis in cancer cells. MTHFD1/2-IN-1 exhibits favorable Caco-2 permeability and hepatic microsomal metabolic stability. MTHFD1/2-IN-1 shows significant anti-leukemic activity, which not only reduces the viability of various leukemia cells but also inhibits tumor growth of acute myeloid leukemia (AML) in mouse models .
Cat. No.: HY-110102
CAS No.: 130065-61-1
Synonyms: Azaspirane hydrochloride; SKF 106615-12 hydrochloride; SKF 106615
Research Areas:
Atiprimod (Azaspirane) hydrochloride is a STAT3 inhibitor with antitumor, anti-inflammatory, and anti-angiogenic activities. Atiprimod blocks the signaling pathways of IL-6 and VEGF by inhibiting the phosphorylation of signal transducer and activator of STAT3. Atiprimod blocks the JAK-STAT signaling pathway by inhibiting the phosphorylation of JAK2 and JAK3. Atiprimod also inhibits cell proliferation, induces cell cycle arrest, and induces autophagy and apoptosis. Atiprimod triggers persistent ER stress-mediated apoptosis in breast cancer cells by activating the PERK/eIF2α/ATF4/CHOP axis and inhibiting the nuclear translocation of STAT3/NF-κB. Atiprimod shows great anti-tumor activities in tumor xenograft mouse models. Atiprimod can be used for the study of pituitary adenoma, breast cancer, multiple myeloma and acute myeloid leukemia (AML) .
Cat. No.: HY-13559
CAS No.: 123018-47-3
Synonyms: Azaspirane ; SKF 106615-12; SKF 106615A12
Target:
STAT Apoptosis Autophagy Reactive Oxygen Species (ROS) Caspase Bcl-2 Family p62 Atg8/LC3 PARP NF-κB PERK JAK
Research Areas:
Atiprimod (Azaspirane) is a STAT3 inhibitor with antitumor, anti-inflammatory, and anti-angiogenic activities. Atiprimod blocks the signaling pathways of IL-6 and VEGF by inhibiting the phosphorylation of signal transducer and activator of STAT3. Atiprimod blocks the JAK-STAT signaling pathway by inhibiting the phosphorylation of JAK2 and JAK3. Atiprimod also inhibits cell proliferation, induces cell cycle arrest, and induces autophagy and apoptosis. Atiprimod triggers persistent ER stress-mediated apoptosis in breast cancer cells by activating the PERK/eIF2α/ATF4/CHOP axis and inhibiting the nuclear translocation of STAT3/NF-κB. Atiprimod shows great anti-tumor activities in tumor xenograft mouse models. Atiprimod can be used for the study of pituitary adenoma, breast cancer, multiple myeloma and acute myeloid leukemia (AML) .
Cat. No.: HY-13559A
CAS No.: 183063-72-1
Synonyms: Azaspirane dimaleate; SKF 106615-12 dimaleate; SKF 106615A12 dimaleate
Target:
STAT Apoptosis Caspase Interleukin Related Autophagy Reactive Oxygen Species (ROS) Atg8/LC3 p62 JAK
Research Areas:
Atiprimod (Azaspirane) (dimaleate) is a STAT3 inhibitor with antitumor, anti-inflammatory, and anti-angiogenic activities. Atiprimod blocks the signaling pathways of IL-6 and VEGF by inhibiting the phosphorylation of signal transducer and activator of STAT3. Atiprimod blocks the JAK-STAT signaling pathway by inhibiting the phosphorylation of JAK2 and JAK3. Atiprimod also inhibits cell proliferation, induces cell cycle arrest, and induces autophagy and apoptosis. Atiprimod triggers persistent ER stress-mediated apoptosis in breast cancer cells by activating the PERK/eIF2α/ATF4/CHOP axis and inhibiting the nuclear translocation of STAT3/NF-κB. Atiprimod shows great anti-tumor activities in tumor xenograft mouse models. Atiprimod can be used for the study of pituitary adenoma, breast cancer, multiple myeloma and acute myeloid leukemia (AML) .
Cat. No.: HY-149359
CAS No.: 3049485-80-2
Target:
Research Areas:
IHMT-IDH1-053 (compound 16) is a highly selectivity and irreversible IDH1-mutant inhibitor with an IC50 of 4.7 nM for IDH1 R132H. IHMT-IDH1-053 displays high selectivity against IDH1 mutants over IDH1 wt and IDH2 wt/mutants. IHMT-IDH1-053 inhibits 2-hydroxyglutarate (2-HG) production in IDH1 R132H mutant transfected 293T cells (IC50=28 nM). IHMT-IDH1-053 binds to the IDH1 R132H protein in the allosteric pocket adjacent to the NAPDH binding pocket through a covalent bond with residue Cys269. IHMT-IDH1-053 inhibits the proliferation of HT1080 cell line and primary AML cells which both bear IDH1 R132 mutants .
Cat. No.: HY-181078
Target:
Research Areas:
Cephalotaxine-ester-(R)-1-ethoxy-3-mercaptopropan-2-ol-Ph (3,4OMe) is an anti-leukemic agent with potent ribosome-targeting protein synthesis inhibition. Cephalotaxine-ester-(R)-1-ethoxy-3-mercaptopropan-2-ol-Ph (3,4OMe) downregulates short-lived oncoproteins, including c-Myc and Mcl-1, by inhibiting protein synthesis. Cephalotaxine-ester-(R)-1-ethoxy-3-mercaptopropan-2-ol-Ph (3,4OMe) induces cell cycle arrest at the G0/G1 phase and triggers mitochondrial pathway-mediated apoptosis in acute myeloid leukemia (AML) cells. Cephalotaxine-ester-(R)-1-ethoxy-3-mercaptopropan-2-ol-Ph (3,4OMe) is applicable for research on leukemia .
Cat. No.: HY-177578
Research Areas:
NN3201 is a c-Kit-targeting antibody-drug conjugate (ADC) with high affinity (KD = 0.19 pM). NN3201 is composed of 4-(3-Tosyl-2-(tosylmethyl)propanoyl)benzoic acid-glu(PEG24-Me)-val-cit-NH-benzyloxyformic acid-MMAE (HY-178219) and an anti-c-Kit human monoclonal antibody NN2101 (HY-P991293). NN3201 rapidly internalizes and inhibits stem cell factor (SCF)-driven signaling, thereby delivering its payload to induce cell cycle arrest and apoptosis. NN3201 exhibits no Fc-mediated effector functions antibody-dependent cell-mediated cytotoxicity (ADCC)/complement-dependent cytotoxicity (CDC) due to reduced FcγR binding. NN3201 exhibits significant c-Kit-dependent anti-tumor efficacies in various tumor models. NN3201 can be used in small cell lung cancer (SCLC) and gastrointestinal stromal tumor (GIST) and acute myeloid leukemia (AML) research [1][2].
Cat. No.: HY-178858
Research Areas:
PROTAC FLT3/CHK1 Degrader-1 is a PROTAC FLT3/CHK1 degrader, with DC50 values of 5.88 nM (FLT3) and 4.17 nM (CHK1), respectively. PROTAC FLT3/CHK1 Degrader-1 can inhibit the phosphorylation of FLT3 downstream signaling effectors STAT5 (Tyr694), AKT (Ser473), and ERK (Tyr204), downregulate the protein level of c-Myc and maintain the expression of p53 protein. PROTAC FLT3/CHK1 Degrader-1 induces Apoptosis in cells. PROTAC FLT3/CHK1 Degrader-1 shows significant anti-tumor efficacy in mice bearing MV-4-11 subcutaneous xenografts. PROTAC FLT3/CHK1 Degrader-1 can be used for the study of acute myeloid leukemia (AML) .
Cat. No.: HY-121708
CAS No.: 930089-25-1
KI-328 is a novel inhibitor targeting KIT kinase that has selective activity against some KIT mutant kinases commonly found in acute myeloid leukemia (AML). KI-328 showed specificity for KIT kinase in in vitro kinase assays and inhibited the growth of wild-type (Wt) and mutant KIT-expressing cells, but had lower activity against D816V-KIT. Comparative analysis of the inhibitory effects of several potent KIT inhibitors on the growth of multiple mutant KIT-expressing cells showed that the multi-kinase inhibitors had comparable activity against D816V-KIT as against other mutant KITs; however, heat shock protein 90 (HSP90) inhibitors showed significant activity against D816V-KIT, inhibiting the growth of D816V-KIT-expressing cells at concentrations that did not affect the growth of other mutant KIT-expressing cells. These results suggest that potent KIT inhibitors have different activities against different types of KIT mutant kinases. Therefore, in clinical development, KIT inhibitors need to validate their activity against multiple types of KIT mutant kinases.
Cat. No.: HY-170576
FLT3-IN-28 (Compound 12y) is an orally active FLT3 inhibitor with antitumor activity. FLT3-IN-28 selectively inhibits cancer cells harboring the FLT3 internal tandem duplication (ITD) mutation, with IC50 values of 85, 290, 130, 65, and 220 nM for BaF3-FLT3-ITD, BaF3-TEL-VEGFR2, MV4-11, MOLM-13, and MOLM-14 cell lines respectively (MV4-11 and MOLM-13/14 are acute myeloid leukemia (AML) cell lines carrying the FLT3-ITD mutation). Additionally, FLT3-IN-28 can downregulate the phosphorylation levels of FLT3 and STAT5 in MOLM-13 cells and induce cell cycle arrest and Apoptosis. FLT3-IN-28 has an oral bioavailability of 19.2% in SD rats and can prolong survival in a dose-dependent manner in NSG mice xenografted with MOLM-13 cells. FLT3-IN-28 holds promise for research in cancer fields related to FLT3-ITD .
-
-
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
