glioblastoma multiforme

Vacquinol-1 is an MKK4 activator, which rapidly and selectively induces glioma cell death.

Duocarmycin SA is an extremely potent cytotoxic agent and antitumor antibiotic that induces sequence-selective alkylation of duplex DNA, with an IC50 of 10 pM. It demonstrates synergistic cytotoxicity against glioblastoma multiforme (GBM) cells when combined with proton radiation in vitro.

RIPGBM is a selective inducer of apoptosis in glioblastoma multiforme cancer stem cells (EC50: ≤500 nM).

PT109 is a multikinase inhibitor that targets JNK and other kinases, playing a crucial role in anti-inflammatory, antioxidative, neurogenic, and synaptogenic processes. Specifically, PT109 inhibits JNK isoforms with the following IC50 values: JNK1 at 0.143 μM, JNK2 at 0.831 μM, and JNK3 at 0.285 μM. It also inhibits SGK isoforms (SGK1: IC50=1.34 μM; SGK2: IC50=5.6 μM; SGK3: IC50=26.4 μM) and ROCK2 (IC50=34 μM). Additionally, PT109 reprograms polymorphic glioblastoma multiforme (GBM) into oligodendroglia via the PTBP1 PKM1 2 pathway and alters the metabolic pattern of GBM to exhibit antiglioma activity.

Ena15 is an ALKBH5 inhibitor that enhances the demethylase activity of FTO. It can increase m6A RNA levels and stabilize FOXM1 mRNA. Additionally, Ena15 inhibits the growth activity of glioblastoma multiforme.

AEE788 (NVP-AEE 788) has been used in trials studying the treatment of Cancer, Glioblastoma Multiforme, and Brain and Central Nervous System Tumors.

Temozolomide Acid (TMZA) is a metabolite of temozolomide (TMZ). Temozolomide processes anticancer activity in vitro. Temozolomide (TMZ) is an oral alkylating agent used to treat glioblastoma multiforme (GBM) and astrocytomas.

Survivin (also known as baculoviral IAP repeat-containing protein 5 (BIRC5)) is a member of the inhibitor of apoptosis (IAP) family that interacts with and inhibits the apoptotic function of several proteins. LLP-3 is a cell-permeable ligand of Survivin that blocks its interaction with Ran, resulting in the induction of apoptosis (IAP) in glioma stem cells (IC50 = 31 μM). It abolishes the growth of glioblastoma multiforme cell in spheres and in tumor slice cultures.

K-TMZ is a DNA alkylating agent. It increases the concentration of O6-methylated deoxyguanosine in U87 glioblastoma multiforme (GBM) cells in a concentration-dependent manner. K-TMZ reduces cell viability of GBM cell lines lacking (IC50s = 18-44 μM) or expressing O6-methylguanine DNA methyltransferase (MGMT; IC50s = 115-240 μM). K-TMZ can cross the blood-brain barrier and increases survival in a Br23c mouse xenograft model of GBM when administered at a dose of 14.9 mg/kg.

N1,N11-Diethylnorspermine (DENSPM), a spermine analog, serves as a potent anticancer agent by activating polyamine catabolism, which in turn triggers cytochrome c release from mitochondria and activates caspase 3. This process ultimately leads to the death of glioblastoma multiforme (GBM) cells by inducing spermidine spermine N1-acetyltransferase (SSAT) activity along with the production of H2O2 [1] [2] [3].

Aurora LIM kinase-IN-1 (Compound F114) is a potent dual inhibitor of aurora and LIM kinases. It inhibits the proliferation and invasion of glioblastoma multiforme (GBM), making it a potential candidate for drug development in GBM and other cancers. Aurora and LIM kinases are involved in neoplastic cell division and cell motility, respectively [1].

PDZ1i is a potent MDA-9 Syntenin-specific inhibitor that crosses the blood-brain barrier. PDZ1i inhibits key GBM (glioblastoma multiforme) signaling, including FAK and EGFRvIII, and reduces MMP secretion.

GPI-15427 is a potent PARP-1 inhibitor capable of crossing the blood-brain barrier, which can significantly increased the antitumor activity of the methylating agent TMZ against malignant melanoma, glioblastoma multiforme, or lymphoma growing at the CNS site. GPI-15427 acts as a potent inhibitor of the enzyme, being capable of inhibiting the activity of purified PARP-1 at nanomolar concentrations. GPI-15427 induced significant sensitization to radiotherapy, representing a promising new treatment in the management of HNSCC.

MDM2-p53-IN-16 is a potent inhibitor of the MDM2-p53 complex, with an IC 50 value of 4.3 nM for the dissociation of the human p53 MDM2 complex. It effectively reactivates p53, leading to apoptosis and cell-cycle arrest in Glioblastoma Multiforme (GBM) cells, positioning it as a valuable agent for cancer research.

Asunercept (APG101; CAN008), a soluble CD95-Fc fusion protein, selectively targets and binds to CD95L, effectively disrupting CD95 CD95L signaling. It is utilized in research for treating glioblastoma multiforme (GBM), myelodysplastic syndrome (MDS), and graft-versus-host disease (GvHD) [1] [2] [3].

4-Borono-L-phenylalanine has antitumor activity and may be used in clinical trials of boron neutron capture therapy for the treatment of melanoma and glioblastoma multiforme.

Tubulin Inhibitor 36 (Compound 10) serves as a potent novel inhibitor of tubulin polymerization, which consequently induces apoptosis in glioblastoma cells, reflected by an IC50 value of 1.5±0.1 μM. Exhibiting significant anti-mitotic activity, this compound demonstrates anti-tumor potential, particularly useful in glioblastoma multiforme (GBM) research [1].

IV-275 is a dual inhibitor targeting the bromodomains of both BRG1 and BRM. This compound not only augments DNA damage when combined with Temozolomide and Bleomycin but also suppresses the invasiveness of GBM cells. Furthermore, IV-275 amplifies Temozolomide-induced cell death and its apoptosis-inducing activity [1].

KSL-128114, a peptide inhibitor of the membrane regulator syntenin (Ki = 300 nM), notably diminishes the viability of A2058 melanoma and patient-derived glioblastoma multiforme (GBM) cells in a concentration-dependent manner. Furthermore, when administered at 50 µM, KSL-128114 elevates survival times in a patient-derived xenograft (PDX) mouse model of GBM, where mice were implanted intracranially with patient-derived GBM cells pre-cultured with KSL-128114.

HYDAMTIQ, a PARP-1 2 inhibitor (IC 50 : 29-38 nM), exhibits a range of pharmacological effects including anticancer, anti-inflammatory, and ischemic protective properties. It effectively reduces pulmonary PARP activity and alleviates symptoms such as allergen-induced cough and dyspnea while also diminishing bronchial hyperresponsiveness to methacholine. Moreover, HYDAMTIQ shows potent tumor suppressor activity in various cancers such as ovarian, breast, prostate, pancreatic, and glioblastoma multiforme. Demonstrating in vivo efficacy, HYDAMTIQ has been tested in animal models for conditions like cerebral ischemia, asthma, and cancer [1].

EGFRvIII peptide PEPvIII acetate is a tumor-specific mutation that is widely expressed in glioblastoma multiforme (GBM) and other neoplasms and enhances tumorigenicity.