Glioblastoma is a highly aggressive and malignant brain tumor arising from astrocytes, characterized by rapid infiltration into surrounding brain tissue, necrosis, abnormal blood vessel formation, and pleomorphic, anaplastic cells. It is the most common and deadly primary brain cancer, with a poor prognosis, often presenting with nonspecific symptoms such as headaches, nausea, drowsiness, personality changes, and stroke-like neurological deficits. While the exact cause remains largely unknown, rare associations exist with genetic syndromes.
| Cat. No. |
Product Name |
CAS No. |
Purity |
Chemical Structure |
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- HY-14909
-
|
Bardoxolone
|
218600-44-3 |
99.50% |
|
Bardoxolone (CDDO; RTA 401) is a Nrf2 activator. Bardoxolone shows anti-SARS-CoV-2 3CLpro with IC50 of 27.99 μM. Bardoxolone activates the Nrf2 pathway and inhibits the NF-κB pathway. Bardoxolone can induce cells differentiation, apoptosis and shows antiproliferative activity against cancer cells. Bardoxolone can increase ROS and decrease intracellular GSH levels. Bardoxolone inhibits Z-VAD-FMK (HY-16658B)-induced necroptosis. Bardoxolone can be used for the research of cancer, inflammation and infection, such as SARS-CoV infection and glioblastoma.
|
-
-
- HY-50722
-
|
NNC 55-0396
|
357400-13-6 |
98.43% |
|
NNC 55-0396 (NNC 55-0396 dihydrochloride) is a blood-brain-barrier-permeable T-type Ca2+ channel inhibitor and pan-P450 inhibitor. NNC 55-0396 selectively inhibits T-type Ca2+ channels, suppresses HIF-1α expression and stability and inhibits Kv currents. NNC 55-0396 reduces brain infarct and attenuates neurological dysfunction. NNC 55-0396 inhibits the activity of multiple P450 enzymes. NNC 55-0396 (free base) can be used for the research of brain injury, hypertension, and glioblastoma.
|
-
-
- HY-12494
-
|
LDC1267
|
1361030-48-9 |
99.64% |
|
LDC1267 is a AXL/TAM/FLT3 inhibitor with IC50 values of 42 nM, 130 nM, and 63 nM against AXL, MERTK, and TYRO3, respectively. LDC1267 blocks GAS6-induced AXL phosphorylation and the downstream AKT/ERK1/2 signaling pathway. LDC1267 inhibits cancer cell proliferation, colony formation, and glioblastoma cell invasion, without causing obvious impairment of cytotoxic autophagic flux. LDC1267 exerts a synergistic effect when used in combination with Imatinib (HY-15463) in chronic myeloid leukemia models. LDC1267 can be widely applied in studies related to glioblastoma and chronic myeloid leukemia.
|
-
-
- HY-16397
-
|
Phenformin
|
114-86-3 |
98.02% |
|
Phenformin (Phenethylbiguanide) is an orally active biguanide hypoglycemic agent. Phenformin inhibits mitochondrial respiratory chain complex I, leading to an increased AMP/ATP ratio, activation of AMPK, and subsequent inhibition of the mTOR pathway, thereby suppressing cell proliferation, inducing apoptosis and autophagy. Phenformin inhibits cancer stem cells (CSCs) and possesses potent antitumor potential.
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-
-
- HY-100685
-
|
MS-444
|
150045-18-4 |
99.42% |
|
MS-444 (BE-34776) is a HuR (ELAVL1) inhibitor that blocks the cytoplasmic translocation of HuR and inhibits its dimerization. MS-444 reduces cytoplasmic HuR levels by preventing the binding of HuR to ARE-mRNA, without altering the total expression of HuR. MS-444 induces apoptosis, inhibits cell growth, angiogenesis and invasion, and also regulates immune function and microbiota. MS-444 effectively alters the number, size and invasiveness of tumors in various cancer models. MS-444 is tolerable to intraperitoneal injection in vivo and can be applied to research related to colorectal cancer, familial adenomatous polyposis, colitis-associated cancer and glioblastoma.
|
-
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- HY-Q66655
-
|
YRDC-IN-1
|
3120494-74-5 |
|
|
YRDC-IN-1 is a blood-brain barrier-permeable YRDC inhibitor. YRDC is a key enzyme that catalyzes the formation of N6-threonylcarbamoyladenosine at position 37 of tRNA (t6A37). YRDC-IN-1 selectively inhibits the translation of ANN codon-enriched FABP7, thereby reducing lipid droplet formation, increasing ROS, and reversing the acquired resistance of GBM to Temozolomide (TMZ) (HY-17364). YRDC-IN-1 can be used for the research of glioblastoma.
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-
- HY-W010480
-
|
Toluquinone
|
553-97-9 |
|
|
Toluquinone is a Toluquinol analogue. Toluquinone shows lower growth inhibitory activity against a panel of cancer cell lines of breast adenocarcinoma, promyelocytic leukemia, glioblastoma, fibrosarcoma, and colorectal adenocarcinoma than Toluquinol.
|
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- HY-129040
-
|
m-Iodobenzylguanidine
|
80663-95-2 |
|
|
m-Iodobenzylguanidine (Iobenguane) is a ligand with high affinity against norepinephrine transporter (NET). m-Iodobenzylguanidine is used as an imaging agent in the diagnostic imaging and radionuclide studies of neuroendocrine tumors, such as neuroblastoma, pheochromocytoma and carcinoid tumor.
|
-
-
- HY-W011725
-
|
N-6-Methyl-2-deoxyadenosine
|
2002-35-9 |
99.83% |
|
N-6-Methyl-2-deoxyadenosine (m6dA) is an adenine nucleoside analogue. N-6-Methyl-2-deoxyadenosine targets nuclear processes and DNA replication machineries including WER, SATB1, TFAM, Jumu, SSBP1, DNA polymerase η and phage polymerase Gp90 exo−. N-6-Methyl-2-deoxyadenosine acts as a multifunctional epigenetic regulator that modulates transcription, DNA damage response, cell cycle, transposon silencing, stress adaptation, epigenetic crosstalk, and nucleosome organization in both prokaryotes and eukaryotes. N-6-Methyl-2-deoxyadenosine regulates mitochondrial epigenetic inheritance and is required for fear extinction memory in mice. N-6-Methyl-2-deoxyadenosine exhibits dysregulated levels in cancers. N-6-Methyl-2-deoxyadenosine can be used for the research of glioblastoma, triple negative breast cancer, and conditioned fear (fear extinction impairment).
|
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- HY-125848
-
|
Ginsenoside F2
|
62025-49-4 |
99.92% |
|
Ginsenoside F2 is an orally active bioactive compound that participates in the regulation of metabolism and inflammation. Ginsenoside F2 promotes the phosphorylation of AMPK and ACC, binds to PPARγ, inhibits the phosphorylation of MAPK, activates the PI3K/AKT/GSK-3β pathway, reduces GLRX expression, and regulates lipid metabolism. Ginsenoside F2 reduces ROS production and MDA levels, restores SOD activity in cells, and alleviates oxidative stress. Ginsenoside F2 induces cell apoptosis (Apoptosis) and increases the number of cleaved caspase-3-positive cells. Ginsenoside F2 reduces body weight gain, adipose tissue weight and serum lipid levels in obese mice, and activates the hepatic AMPK signaling pathway and the expression of antioxidant enzymes. Ginsenoside F2 alleviates atopic dermatitis in mice by inhibiting inflammation and reshaping the gut microbiota. Ginsenoside F2 is applicable to research related to insulin resistance, obesity, atopic dermatitis, liver cancer, glioblastoma and glioma.
|
-
-
- HY-W019724
-
|
2,2-Dihydroxyacetic acid
|
563-96-2 |
98.0% |
|
2,2-Dihydroxyacetic acid is an endogenous metabolite, which is the monohydrate of Glyoxylic Acid. 2,2-Dihydroxyacetic acid may participate in the microbial glyoxylate cycle, induce an increase in reactive oxygen species, promote cell differentiation, and modify proteins to form advanced glycation end products (AGEs) (HY-NP165). 2,2-Dihydroxyacetic acid is associated with metabolic diseases such as primary hyperoxaluria.
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- HY-172723
-
|
DSPE-PEG2000-T7
|
|
|
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DSPE-PEG2000-T7 is a PEGylated compound composed of DSPE and peptideT7. T7 (HAIYPRH) specifically binds to TfR. DSPE-PEG2000-T7 can be used to prepare T7-modified liposomes, where liposomes modified with both T7 and DA7R peptides can effectively co-deliver Doxorubicin (HY-15142A) and Vincristine (HY-N0488A) to gliomas. DSPE-PEG2000-T7 can also be used to prepare nanomodulators that mediate the co-delivery of tyrosine hydroxylase mRNA and interferon gene stimulator antagonists for synergistic intervention in Parkinson's disease.
|
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- HY-131943
-
|
DS44960156
|
2361327-08-2 |
≥99.0% |
|
DS44960156 is a selective MTHFD2 inhibitor with moderate to low blood-brain barrier penetration (IC50=1.6 μM, Ki=1.23 μM). DS44960156 specifically binds to the active site of MTHFD2, disrupts redox homeostasis and blocks serine-mediated one-carbon metabolism, thereby increasing the NAD+/NADH ratio and ROS levels. DS44960156 not only effectively inhibits the proliferation of glioma cells, but also enhances the sensitivity of cells to glutamine starvation-induced death. DS44960156 binds to plasma proteins, shows no mutagenicity, carcinogenicity or acute oral toxicity, and serves as a research agent for glioblastoma multiforme and other cancers.
|
-
-
- HY-P11099
-
|
Cys-LT7
|
1254540-73-2 |
99.90% |
|
Cys-LT7 is a transferrin receptor (TfR)-targeting peptide ligand. Cys-LT7 binds to a TfR site distinct from endogenous transferrin, mediates conjugated Doxorubicin (HY-15142A) delivery to TfR-overexpressed tumor cells, and exhibits low toxicity to TfR-low-expressed normal cells. Cys-LT7 is an L-configuration peptide susceptible to proteolytic enzymes, leading to poor biostability in peptide-drug conjugates. Cys-LT7 can be used for the research of glioblastoma, hepatocellular carcinoma, lung carcinoma.
|
-
-
- HY-114243
-
|
DpC
|
1382469-39-7 |
98.73% |
|
DpC is a selective, orally active iron chelator with anticancer activity. DpC acts on signaling pathway-related targets such as JNK, NF-κB, and its activity is competitively inhibited by another iron chelator Dp44mT (HY-18973). By chelating intracellular iron and copper ions in tumor cells to form redox-active complexes, DpC induces oxidative stress, activates the JNK, NF-κB pathways and downregulates IκBα, upregulates the expressions of neuroglobin and cytoglobin, activates caspase 3/9 to induce tumor cell apoptosis. It also overcomes P-glycoprotein-mediated multidrug resistance through a lysosome-targeting mechanism, and exhibits broad-spectrum synergistic effects when combined with various chemotherapeutic agents. DpC inhibits tumor metastasis and increases TNF-α levels in the tumor microenvironment to enhance endogenous immune responses. DpC is applicable to the research of various malignancies including neuroblastoma, pancreatic cancer, prostate cancer, lung cancer, and breast cancer.
|
-
-
- HY-129440
-
|
N-(p-Coumaroyl) Serotonin
|
68573-24-0 |
99.03% |
|
N-(p-Coumaroyl) Serotonin is an orally active polyphenol found in safflower seeds with potent anti-inflammatory, antioxidant, and antitumor activities. N-(p-Coumaroyl) Serotonin suppresses NF‑κB, TLR4/MyD88 and MAPK signaling, activates NQO1/HO‑1 pathways, and inhibits pro‑inflammatory cytokines, iNOS and COX‑2 and ROS production. N-(p-Coumaroyl) Serotonin induces S‑phase arrest and apoptosis in glioblastoma cells, reduces atherosclerotic lesions, and alleviates renal and vascular injuries. N-(p-Coumaroyl) Serotonin acts as a vasodilator, regulates calcium dynamics. N-(p-Coumaroyl) Serotonin can be used for the research of neurodegenerative diseases, atherosclerosis, glioblastoma, and acute renal failure.
|
-
-
- HY-175200
-
|
DEL-S1
|
|
98.50% |
|
DEL-S1 is a SLIT2 binder. DEL-S1 significantly inhibits the formation of the SLIT2/ROBO1 complex by inducing conformational rearrangement, and further suppresses its function, with an IC50 of 68.8 μM. DEL-S1 can be used in studies of neurodevelopment, immunomodulation, and cancers such as glioblastoma.
|
-
-
- HY-167832
-
|
PT109
|
2059104-90-2 |
99.20% |
|
PT109 is an orally active, blood-brain barrier permeable multi-kinase inhibitor. By inhibiting PTBP1, PT109 promotes the switch of pyruvate kinase isoform from PKM2 to PKM1, thereby effectively inhibiting the proliferation and migration of glioblastoma multiforme and inducing its reprogramming into oligodendrocytes. PT109 also targets and regulates key signaling molecules such as JNK, SGK1, GSK3β to exert neuroprotective effects including promoting neurogenesis, inducing synapse formation and alleviating neuroinflammation. In Alzheimer's disease models, PT109 exhibits significant efficacy in improving spatial learning ability, along with excellent in vivo pharmacokinetic properties. PT109 can be used to investigate metabolic reprogramming of glioblastoma multiforme and neuroprotective mechanisms of Alzheimer's disease.
|
-
-
- HY-P11303
-
|
PADRE peptide
|
161147-59-7 |
98.28% |
|
PADRE peptide is a pan-HLA-DR binding epitope and immunostimulant. PADRE peptide binds to the peptide-binding groove of MHC class II molecules for presentation to CD4+ T cells, thereby effectively stimulating specific immune responses. PADRE peptide not only enhances anti-tumor immune responses, inhibits tumor growth and prolongs survival; it also significantly increases the frequency of E7-specific CD8+ T cells and improves therapeutic efficacy against TC-1 tumors when used in combination with E7 peptide-based vaccines and poly (I:C). The intensity of the immune response induced by PADRE peptide is lower than that of the Ii-PADRE DNA vaccine, and it fails to enhance the immune effect of CRT-E7 DNA. PADRE peptide is widely applicable to research on related tumors such as melanoma, glioblastoma and cervical cancer.
|
-
-
- HY-W587427
-
|
D-2-Phosphoglyceric acid trisodium
|
70195-25-4 |
98.13% |
|
D-2-Phosphoglyceric acid trisodium is a glycolysis and gluconeogenesis intermediate with altered levels linked to MCT4-modulated glycolytic pathways. D-2-Phosphoglyceric acid trisodium shows reduced intracellular levels in hypoxic glioblastoma stem cells after MCT4 knockdown. D-2-Phosphoglyceric acid trisodium can be used for the research of glioblastoma.
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