2. Cancer
  3. Cancer Metabolism and Metastasis

Cancer Metabolism and Metastasis

Metabolic abnormalities are a major feature of cancer, such as increased substance anabolic pathways and aerobic glycolysis. Cancer metabolism shows flexibility and plasticity, which are crucial for the survival and growth of cancer cells. Cancer metastasis is completed in five steps i.e. invasion, dissemination, circulating tumor cells, colonization, and secondary tumor formation. Recently, metabolic adaptation mechanism of cancer metastasis has been proposed to reveal the extensive relationship between cancer metabolism and cancer metastasis. Metastasizing cancer cells selectively and dynamically adapt their metabolism during the complex multistep cascade.

Many nutrients can promote metabolite plasticity during metastasis. For example, lactic acid and pyruvate are the nutrients that cells can directly absorb from the environment; many cancer cells take up glutamine, which contributes to non-essential amino acid as well as nucleotide synthesis through nitrogen or carbon metabolism. Inhibiting the function of key enzymes in metabolic pathways can in turn inhibit the proliferation of cancer cells. For example, lactate dehydrogenase A or B (LDH-A or -B) knockdown can inhibit breast cancer cell motility in vitro. Oncogenic signaling pathways, such as Myc, phosphoinositide 3-kinase (PI3K)/AKT pathway, MAPK/ERK pathway, LKB1/AMPK pathway and Hippo pathways, mediate metabolic gene expression and increase metabolic enzyme activities.

Cancer Metabolism and Metastasis Related Products (50745):

Cat. No. Product Name CAS No. Purity Chemical Structure
  • HY-B1428
    2-Ethoxybenzamide 938-73-8 99.82%
    2-Ethoxybenzamide (Ethenzamide) is a nonsteroidal anti-inflammatory agent that shows analgesic and antipyretic effects. 2-Ethoxybenzamide induces melanin synthesis via cAMP response element-binding protein (CREB) phosphorylation. 2-Ethoxybenzamide can be used in the research of hypopigmentation and inflammation-related diseases.
    2-Ethoxybenzamide
  • HY-P10087
    Mouse TREM-1 SCHOOL peptide 1292755-24-8 99.91%
    Mouse TREM-1 SCHOOL peptide (Mouse TREM-1(213-221), GF9) targets the interaction between TREM-1 and its signaling partner DAP-12, specifically silencing the TREM-1 signaling pathway, regulate the production of TREM-1-mediated pro-inflammatory cytokines in vivo and in vitro. Mouse TREM-1 SCHOOL peptide has anti-tumor effects. Mouse TREM-1 SCHOOL peptide can reduce the formation of vitreoretinal neovascularization.
    Mouse TREM-1 SCHOOL peptide
  • HY-R00276
    hsa-miR-142-3p mimic 98.71%
    hsa-miR-142-3p mimics are small, chemically synthesized double-stranded RNAs that mimic endogenous miRNAs and enable miRNA functional analysis by up-regulation of miRNA activity.
    hsa-miR-142-3p mimic
  • HY-124776
    NPD8733 696655-62-6 99.92%
    NPD8733 is an inhibitor of cancer cell-enhanced fibroblast migration. NPD8733 specifically binds to valosin-containing protein (VCP)/p97, a member of the ATPase-associated with diverse cellular activities (AAA+) protein family. NPD8733 has the potential for the research of cancer diseases.
    NPD8733
  • HY-P10943
    APO-15 3051946-11-0 99.45%
    APO-15 is a phosphatidylserine-binding fluorescent probe and apoptosis imaging reagent. APO-15 exhibits high chemical stability under proteolytic and oxidative conditions, enables quantification and imaging of drug-induced apoptosis in preclinical mouse models, and is applicable to fixed tissue samples and multiple in vivo administration routes (Ex = 488 nm; Em = 525 nm). APO-15 can be used in studies related to acute lung injury and breast cancer.
    APO-15
  • HY-N8481
    3,6-Dihydroxyflavone 108238-41-1 98.06%
    3,6-Dihydroxyflavone is an anti-cancer agent. 3,6-Dihydroxyflavone dose- and time-dependently decreases cell viability and induces apoptosis by activating caspase cascade, cleaving poly (ADP-ribose) polymerase (PARP). 3,6-Dihydroxyflavone increases intracellular oxidative stress and lipid peroxidation.
    3,6-Dihydroxyflavone
  • HY-119390
    AA-CW236 1869921-96-9 99.9%
    AA-CW236 is a MGMT (O6-methylguanine DNA methyltransferase) inhibitor. AA-CW236 targets MGMT active site Cys145 for covalent modification.
    AA-CW236
  • HY-139664B
    (S)-GSK-3685032 2170142-58-0 98.82%
    (S)-GSK-3685032 is the isomer of GSK-3685032 (HY-139664), and can be used as an experimental control. GSK-3685032 is a non-time-dependent, noncovalently, first-in-class reversible DNMT1-selective inhibitor, with an IC50 of 0.036 μM. GSK-3685032 induces robust loss of DNA methylation, transcriptional activation, and cancer cell growth inhibition.
    (S)-GSK-3685032
  • HY-111595
    SAHA chloroalkane T1 1613617-05-2
    SAHA chloroalkane T1 is a chloroalkane capture tag by tethering Vorinostat (SAHA) and a chloroalkane tag T1.
    SAHA chloroalkane T1
  • HY-156580
    WRN inhibitor 4 2923009-45-2 99.40%
    WRN inhibitor 4 is a Werner Syndrome ATP-dependent helicase (WRN) inhibitor. WRN inhibitor 4 can be used for cancer research.
    WRN inhibitor 4
  • HY-12652
    AZD3147 1101810-02-9 99.93%
    AZD3147 is a potent, orally active, selective dual inhibitor of mTORC1 and mTORC2 with an IC50 value of 1.5 nM. AZD3147 also has a selective effect on PI3K.
    AZD3147
  • HY-167846
    YLIU-4-105-1 2417685-83-5 99.39%
    YLIU-4-105-1 is a Type II JAK2 inhibitor. YLIU-4-105-1 binds to the ATP-binding pocket of JH1. YLIU-4-105-1 has in vivo pharmacodynamic activity as evidenced by inhibiting pSTAT5, reducing spleen to body weight, and lowering blood reticulocyte counts in a dose-dependent manner.
    YLIU-4-105-1
  • HY-W018604
    2,3,5-Tri-O-benzyl-D-ribono-1,4-lactone 55094-52-5 99.97%
    2,3,5-Tri-O-benzyl-D-ribono-1,4-lactone is a purine nucleoside analog. 2,3,5-Tri-O-benzyl-D-ribono-1,4-lactone can be synthesized from D-ribose by reacting with methanol under Fischer glycosylation conditions. Purine nucleoside analogs have broad antitumor activity targeting indolent lymphoid malignancies. 2,3,5-Tri-O-benzyl-D-ribono-1,4-lactone exerts anticancer activities through inhibition of DNA synthesis, induction of apoptosis, etc. 2,3,5-Tri-O-benzyl-D-ribono-1,4-lactone can be studied in anticancer research for lymphoid malignancies.
    2,3,5-Tri-O-benzyl-D-ribono-1,4-lactone
  • HY-P3486
    GADGVGKSAL 199477-24-2 99.93%
    GADGVGKSAL is a mutant KRAS G12D 10mer peptide. GADGVGKSAL can be used as an immunogenic neoantigen for cancer immunotherapy research.
    GADGVGKSAL
  • HY-P4675
    LHRH free acid 35263-73-1 99.68%
    LHRH (free acid), the luteinizing hormone-releasing hormone, is a neuropeptide hypothalamic. LHRH regulates reproduction. LHRH can be used for the research of cancer.
    LHRH free acid
  • HY-180132
    PROTAC AURKA degrader 2 3093582-13-6 98.36%
    PROTAC AURKA degrader 2 (compound D) is a potent and selective PROTAC AURKA degrader with an IC50 of 3.58 nM. PROTAC AURKA degrader 2 exhibits 21.6-fold selectivity for AURKA over AURKB (IC50 = 77.2 nM). PROTAC AURKA degrader 2 specifically depletes AURKA on the mitotic spindle.
    PROTAC AURKA degrader 2
  • HY-50878S
    Crizotinib-d5 1395950-84-1 99.60%
    Crizotinib-d5 is the deuterium labeled Crizotinib. Crizotinib (PF-02341066) is an orally bioavailable, ATP-competitive ALK and c-Met inhibitor with IC50s of 20 and 8 nM, respectively. Crizotinib inhibits tyrosine phosphorylation of NPM-ALK and tyrosine phosphorylation of c-Met with IC50s of 24 and 11 nM in cell-based assays, respectively. Crizotinib is also a ROS1 inhibitor. Crizotinib has effective tumor growth inhibition.
    Crizotinib-d<sub>5</sub>
  • HY-156850
    ITF 3756 2247608-27-9 98.55%
    ITF 3756 is a selective, orally active HDAC6 inhibitor. ITF 3756 antagonizes TNF-α-induced activation of the NF-κB pathway. ITF 3756 reduces PD-L1 expression on human monocytes and CD8+ T cells, and exhibits antitumor activity. ITF 3756 can be used in colon cancer-related research.
    ITF 3756
  • HY-N7617
    Toralactone 41743-74-2 98.75%
    Toralactone, isolated from Cassia obtusifolia, mediates hepatoprotection via an Nrf2-dependent anti-oxidative mechanism.
    Toralactone
  • HY-176792
    ACBI-4 3097985-19-5 98.01%
    ACBI-4 is a selective GTP-loaded active state of KRAS (KRAS(on)) PROTAC degrader, with Kd values of 141 nM against KRASG12R. ACBI-4 forms a stable ternary complex with VHL, triggering ubiquitination and KRAS degradation via the ubiquitin-proteasome system. ACBI-4 induces antiproliferative effects in KRAS mutant-driven cancer cells. ACBI-4 can be used for the research of KRAS mutant-driven cancer.
    ACBI-4