Neuroblastoma

Idasanutlin (RG7388) is an orally bioavailable MDM2 inhibitor with an IC₅₀ of 6 nM. Idasanutlin disrupts MDM2-p53 binding, stabilizes and activates p53, triggering cell cycle arrest, apoptosis, and reduced cancer cell viability. Idasanutlin reduces EGFR protein expression and phosphorylation, suppresses downstream SHP2, MEK1/2, ERK1/2, AKT, mTOR, p70(S6K1), and S6 signaling. Idasanutlin induces mitochondrial ROS production, drives p38 MAPK phosphorylation, upregulates NOXA, and mediates caspase-3-dependent apoptosis and gasdermin E-mediated pyroptosis. Idasanutlin can be used for the research of TP53-mutant non-small cell lung cancer, T-cell acute lymphoblastic leukemia, colorectal carcinoma, melanoma, diffuse large B-cell lymphoma, mantle cell lymphoma, non-Hodgkin lymphoma, severe fever with thrombocytopenia syndrome, neuroblastoma, acute lymphoblastic leukemia, relapsed or refractory acute myeloid leukemia, osteosarcoma, solid tumors, and hematological tumors.

Omburtamab (Mab 8H9) is a mouse monoclonal immunoglobulin G1 (IgG1) antibody targeting B7-H3. Omburtamab specifically binds to the glycoprotein antigen B7-H3, which is widely expressed on the surface of tumor cells. As a targeting carrier for recombinant toxins, it delivers PE38 to inhibit cellular protein synthesis and induce cytotoxicity in antigen-expressing cancer cells. Omburtamab can be used in research related to glioma, breast cancer, osteosarcoma and neuroblastoma.

JQAD1 is a EP300 PROTAC degrader. JQAD1 selectively targets EP300 and induces its degradation via the CRBN-dependent proteasomal pathway. JQAD1 reduces the levels of H3K27ac and the expression of MYCN. JQAD1 induces apoptosis (apoptosis) and inhibits cancer cell growth. JQAD1 exerts anti-neuroblastoma effects in vivo in a CRBN-dependent manner. JQAD1 can be used for the research of neuroblastoma.

SK-3-91 is a multi-kinase PROTAC degrader that induces the degradation of the maximum number of unique kinases (over 125 distinct kinases) simultaneously. SK-3-91 induces protein degradation via the ubiquitin biotinylation (E-STUB) pathway, such as inducing the degradation of YTHDF2. SK-3-91 also inhibits cell proliferation and induces cell morphological changes. SK-3-91 can be used in research related to acute lymphoblastic leukemia, multiple myeloma, neuroblastoma, ovarian cancer, mantle cell lymphoma, and gastric cancer.

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.

ALK protein ligand-1-PEG2-N3 is an ALK ligand intermediate with a PEG2 linker, which can be used to synthesize ALK-targeting PROTAC degraders (HY-122582). ALK protein ligand-1-PEG2-N3 is applicable to research related to non-small cell lung cancer, anaplastic large cell lymphoma, and neuroblastoma.

ALK ligand-2 (compound 3) is a ALK ligand that can be used to synthesize PROTAC degraders targeting ALK (HY-122582). ALK ligand-2 is applicable to research related to non-small cell lung cancer, anaplastic large cell lymphoma, and neuroblastoma.

ZSL-M028 is an orally active and selective Polo-like kinase 4 (PLK4) inhibitor with an IC₅₀ value of 1.1 nM. ZSL-M028 exhibits anti-tumor activity against TRIM37-amplified neuroblastoma, downregulates SAS6, upregulates FBXW5, induces G2-phase cell cycle arrest and apoptosis, activates the p53 signaling pathway, and inhibits tumor cell colony formation and migration. ZSL-M028 shows significant tumor growth inhibitory activity in the IMR-32 neuroblastoma xenograft model. ZSL-M028 can be used in neuroblastoma-related research.

HLB-0532259 is a Aurora-A/N-Myc PROTAC degrader, with a DC₅₀ of 20.2 nM against Aurora-A in MCF-7 cells; its DC₅₀ values against N-Myc are 179 nM in SK-N-BE (2) cells and 229 nM in Kelly cells, respectively. HLB-0532259 induces apoptosis (apoptosis) in MYCN-amplified neuroblastoma cells and inhibits tumor growth in mouse xenograft models. HLB-0532259 can be used for the research of neuroblastoma.

β-NF-JQ1 is a BRD2/3/4 PROTAC degrader. β-NF-JQ1 recruits the AhR E3 ligase complex to BRD2, BRD3 and BRD4, induces AhR-BRD interaction, and mediates AhR-dependent degradation through the proximity effect between the target protein and AhR. β-NF-JQ1 acts as an antiproliferative and cytotoxic agent that induces anticancer activity associated with BRD protein knockdown. β-NF-JQ1 can be used for research on breast cancer and neuroblastoma.

TO-1187 is a selective HDAC6 PROTAC degrader with a DC₅₀ value of 5.81 nM. TO-1187 degrades HDAC6 via the ubiquitin-proteasome pathway. TO-1187 can be used in the research of multiple myeloma, neuroblastoma, and cervical cancer.

AP-1 is a targeted ALK PROTAC degrader. AP-1 effectively degrades various ALK fusion/mutation forms, including degradation of NPM-ALK (DC₅₀ = 4.6 nM) and EML4-ALK (DC₅₀ = 357.6 nM), and exhibits a typical hook effect at high concentrations. AP-1 inhibits phosphorylation of downstream STAT3, downregulates gene expression in the JAK-STAT pathway, and kills ALK-positive tumor cells via activating the caspase-3-dependent apoptosis pathway. AP-1 shows cytotoxicity against a variety of cancer cells and possesses anti-tumor activity. AP-1 can be used in research related to non-small cell lung cancer, neuroblastoma, and anaplastic large cell lymphoma.

Idasanutlin-d₃-1 (RG7388-d₃-1) is the deuterated-labeled Idasanutlin (HY-15676). Idasanutlin (RG7388) is an orally bioavailable MDM2 inhibitor with an IC₅₀ of 6 nM. Idasanutlin disrupts MDM2-p53 binding, stabilizes and activates p53, triggering cell cycle arrest, apoptosis, and reduced cancer cell viability. Idasanutlin reduces EGFR protein expression and phosphorylation, suppresses downstream SHP2, MEK1/2, ERK1/2, AKT, mTOR, p70(S6K1), and S6 signaling. Idasanutlin induces mitochondrial ROS production, drives p38 MAPK phosphorylation, upregulates NOXA, and mediates caspase-3-dependent apoptosis and gasdermin E-mediated pyroptosis. Idasanutlin can be used for the research of TP53-mutant non-small cell lung cancer, T-cell acute lymphoblastic leukemia, colorectal carcinoma, melanoma, diffuse large B-cell lymphoma, mantle cell lymphoma, non-Hodgkin lymphoma, severe fever with thrombocytopenia syndrome, neuroblastoma, acute lymphoblastic leukemia, relapsed or refractory acute myeloid leukemia, osteosarcoma, solid tumors, and hematological tumors.

TM-2-51 is a HDAC8 activator with a K_d value of 0.28 μM. TM-2-51 inhibits α-glucosidase with an IC₅₀ of 171.21 μM. TM-2-51 upregulates HDAC8 expression, modulates the TP53, STAT3/ERK and PI3K-AKT pathways, alleviates LeTx-induced cell cycle arrest, downregulates JMJD3 and increases H3K27me3 levels. TM-2-51 selectively induces apoptosis in tumor cell and upregulates p53/p21 expression. TM-2-51 inhibits tumor cell proliferation, migration and invasion, induces G₁-phase arrest and suppresses tumor growth in vivo. TM-2-51 can be used in research on osteosarcoma, anthrax, type 2 diabetes and neuroblastoma.

Oleyl alcohol is an anti-tumor compound that inhibits tumor growth. Oleyl alcohol induces cytotoxicity, cell death and apoptosis. The intracellular accumulation of Oleyl alcohol correlates with its cytotoxicity against tumor cells. Oleyl alcohol forms enhancer-enriched fluid domains in stratum corneum lipids, increases the retention of diclofenac diethylamine in ex vivo human epidermis and dermis, and enhances the skin permeability of diclofenac diethylamine. Oleyl alcohol can be used in studies related to neuroblastoma.

N-Myc-IN-1 is a selective N-Myc inhibitor/degrader with a K_d value of 1.47 μM. N-Myc-IN-1 promotes phosphorylation of N-Myc at threonine-58, triggers N-Myc degradation via the ubiquitin-proteasome pathway, and suppresses the expression of N-Myc target genes. N-Myc-IN-1 reduces the viability of MYCN-dependent tumor cells and induces apoptosis. N-Myc-IN-1 can be used in the research of neuroblastoma.

SU11657 (N,N-Dimethyl sunitinib) is an orally active multi-targeted tyrosine kinase inhibitor with IC₅₀ values of 0.04 μM (c-Kit), 0.005 μM (PDGFR), 0.013 μM (VEGFR1), 0.017 μM (VEGFR2) and 50 nM (FLT3), respectively. SU11657 exhibits anti-angiogenic activity. SU11657 delays leukemia progression, synergizes with ATRA (HY-14649) to reduce leukemia burden, and inhibits symptoms and tissue damage associated with rheumatoid arthritis. SU11657 can be used in research related to FLT3-mutated acute promyelocytic leukemia, rheumatoid arthritis, neuroblastoma, and benign/atypical meningioma.

Viriditoxin ((-)-Viriditoxin) is a mycotoxin. Viriditoxin promotes tubulin polymerization, and inhibits FtsZ polymerization and GTPase activity. Viriditoxin exhibits cytotoxicity against cancer cells, induces apoptosis, inhibits cell migration and colony formation, induces G₂/M phase arrest, and triggers autophagic cell death. Viriditoxin activates caspase-3, cleaves PARP, promotes cytochrome c release, and induces ROS production. Viriditoxin possesses broad-spectrum antibacterial activity against Gram-positive pathogenic bacteria, fish pathogenic bacteria, and permeabilized Gram-negative bacteria. Viriditoxin can be used in research related to ovarian cancer, lung cancer, nasopharyngeal carcinoma, colon cancer, neuroblastoma, prostate cancer, leukemia, lymphoma, bacterial infections, and streptococcosis.

FNIII14 is a β1-integrin inhibitory peptide. FNIII14 induces the conformational shift of β1-integrin from the active form to the inactive form, blocks integrin-mediated signaling pathways, disrupts the interaction between VLA-4 and fibronectin, inhibits the phosphorylation of FAK/Akt, suppresses cell adhesion, fibronectin fibril formation and chondrocyte proliferation, induces chondrocyte apoptosis and cartilage degeneration, upregulates the pro-apoptotic protein Bim, and binds to membrane-bound eEF1A. FNIII14 reversibly disrupts cell adhesion without reducing cell viability, accelerates adipocyte differentiation, and loosens tumor matrix architecture to enhance the permeability of nanotherapeutic agents. FNIII14 can be used in research related to neuroblastoma, pancreatic cancer, acute myeloid leukemia, colitis-associated colorectal cancer, osteoarthritis, and atherosclerosis.

YB-3-17 is a blood-brain barrier permeable mTOR inhibitor (IC₅₀ = 0.22 nM) and GSPT1 PROTAC degrader. YB-3-17 inhibits mTORC1/2, CK1δ/ε, mutant ALK and HER2 kinases, induces CRBN-dependent selective GSPT1 degradation, ablates mTOR downstream phosphorylation, downregulates c-Myc/Cyclin D1 to impair tumor translation, triggers p53-mediated apoptosis, suppresses tumor proliferation and xenograft tumor growth, and can be used for the study of glioma, neuroblastoma, breast cancer, lymphoma, colorectal cancer and lung cancer.