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DRUG:

methionine enkephalin (STAT-401)

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Other names: STAT-401, MENK, MET-enkephalin, Opioid Growth Factor, OGF, IRT-101, INNO-105, CYTO-401, STAT-400
Associations
Trials
Company:
Biostax Corp, Statera BioPharma
Drug class:
Immunostimulant, µ-opioid agonist, δ opioid agonist
Related drugs:
Associations
Trials
3ms
Targeting OGF/OGFR Signal to Mitigate Doxorubicin-induced Cardiotoxicity. (PubMed, Free Radic Biol Med)
This study revealed a substantial increase in circulating levels of opioid growth factor (OGF) (also known as methionine enkephalin) and myocardial expression levels of both OGF and its receptor (OGFR) in subjects treated with doxorubicin (Dox)...Conversely, OGF supplementation exacerbated DIC manifestations, which could be abolished by administration of the OGFR antagonist naltrexone (NTX)...The pretreatment of tumor-bearing mice with the assembled NTX nanodrug successfully provided cardioprotection against Dox toxicity without affecting Dox therapy in tumors. Taken together, this study provides a novel understanding of Dox cardiotoxicity and sheds light on the development of cardioprotectants for patients with tumors receiving Dox treatment.
Journal
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STAT1 (Signal Transducer And Activator Of Transcription 1) • FTL (Ferritin Light Chain)
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doxorubicin hydrochloride • methionine enkephalin (STAT-401) • naltrexone
4ms
Effects of Pain Relief Through Minimal Exercise Intervention in a Rat Model of Neuropathic Pain. (PubMed, Cureus)
In the brain, we examined the increased expression of β-endorphin/met-enkephalin in the gray matter of the midbrain aqueduct...In the midbrain, the Ex group showed a significant increase compared to the No-Ex group. In summary, our results suggest that in minimal-exercise intervention, neuropathic pain relief is achieved by activation of the descending pain inhibitory system in the midbrain.
Preclinical • Journal
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TNFA (Tumor Necrosis Factor-Alpha) • CCR2 (C-C Motif Chemokine Receptor 2) • BDNF (Brain Derived Neurotrophic Factor) • GFAP (Glial Fibrillary Acidic Protein) • TRAF6 (TNF Receptor Associated Factor 6)
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methionine enkephalin (STAT-401)
10ms
The Opioid Receptor Influences Circadian Rhythms in Human Keratinocytes through the β-Arrestin Pathway. (PubMed, Cells)
To investigate this link, we conducted a 48 h circadian rhythm experiment, during which RNA samples were collected every 5 h. We discovered that the activation of DOPr by its endogenous agonist Met-Enkephalin in N/TERT-1 keratinocytes, synchronized by dexamethasone, resulted in a statistically significant 5.6 h delay in the expression of the core clock gene PER2. In summary, our findings suggest that DOPr activation leads to a phase shift in PER2 expression via β-arrestin-1-facilitated chromatin remodeling. Consequently, these results indicate that DOPr, much like its role in wound healing, may also play a part in cancer development by influencing PER2.
Journal
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PER2 (Period Circadian Regulator 2) • CLOCK (Clock Circadian Regulator)
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dexamethasone • methionine enkephalin (STAT-401)
almost1year
In vitro and in vivo killing effects of methionine enkephalin on osteosarcoma. (PubMed, Int Immunopharmacol)
MENK reduces the abundance of myeloid-derived suppressor cells, induces M1 polarization of macrophages, and exhibits an inhibitory effect on osteosarcoma.
Preclinical • Journal • PARP Biomarker • IO biomarker
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BCL2 (B-cell CLL/lymphoma 2) • TNFA (Tumor Necrosis Factor-Alpha) • PARP1 (Poly(ADP-Ribose) Polymerase 1) • IL10 (Interleukin 10) • BAX (BCL2-associated X protein) • CASP3 (Caspase 3) • ITGAM (Integrin, alpha M) • CASP9 (Caspase 9)
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BCL2 expression
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methionine enkephalin (STAT-401)
1year
Methionine enkephalin inhibited cervical cancer migration as well as invasion and activated CD11b NCR1 NKs of tumor microenvironment. (PubMed, Int Immunopharmacol)
Through in vivo mouse model, we found that menk IFNγ and NKP46 expression was upregulated in tumor tissues by menk compared with controls, while LAG3 expression was inhibited by menk, besides, there was an upregulation of CD11b NCR1 NKs of tumor microenvironment in cervical cancer. Therefore, we concluded that menk inhibited cancer migration and invasion via affecting EMT related indicators and activated CD11b NCR1 NKs of tumor microenvironment in cervical cancer, laying a theoretical foundation for the further clinical treatment of menk.
Journal • IO biomarker
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IFNG (Interferon, gamma) • LAG3 (Lymphocyte Activating 3) • CDH1 (Cadherin 1) • VIM (Vimentin) • ITGAM (Integrin, alpha M) • CDH2 (Cadherin 2) • NCR1 (Natural Cytotoxicity Triggering Receptor 1)
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LAG3 expression • IFNG expression
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methionine enkephalin (STAT-401)
over1year
Methionine enkephalin suppresses lung cancer metastasis by regulating the polarization of tumor-associated macrophages and the distribution of myeloid-derived suppressor cells in the tumor microenvironment and inhibiting epithelial-mesenchymal transition. (PubMed, Int Immunopharmacol)
MENK reduced the number of M2 macrophages and MDSC infiltration, and downregulated the expression of interleukin-10 and transforming growth factor-β1 in both primary and metastatic tumors of nude mice. The present findings suggest that MENK is a potential target for suppressing metastasis in lung cancer treatment.
Journal
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IL10 (Interleukin 10) • TGFB1 (Transforming Growth Factor Beta 1)
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methionine enkephalin (STAT-401)
2years
Methionine enkephalin inhibits colorectal cancer by remodeling the immune status of the tumor microenvironment. (PubMed, Int Immunopharmacol)
These finding indicate that MENK remodels the TIME in CRC to inhibit tumor progression by binding to OGFr. MENK is a potential therapeutic agent for CRC, especially for improving the efficacy of immunotherapy.
Journal • PD(L)-1 Biomarker • IO biomarker
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PD-L1 (Programmed death ligand 1) • KRAS (KRAS proto-oncogene GTPase) • BCL2 (B-cell CLL/lymphoma 2) • PD-1 (Programmed cell death 1) • IFNG (Interferon, gamma) • IL6 (Interleukin 6) • LAG3 (Lymphocyte Activating 3) • BCL2L1 (BCL2-like 1) • TNFA (Tumor Necrosis Factor-Alpha) • IL10 (Interleukin 10) • GZMB (Granzyme B) • IL17A (Interleukin 17A) • IL1B (Interleukin 1, beta)
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PD-L1 expression • PD-1 expression
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methionine enkephalin (STAT-401)
over2years
Methionine enkephalin inhibited cervical carcinoma via apoptosis promotion and reduction of myeloid derived suppressor cell infiltrated in tumor. (PubMed, Int Immunopharmacol)
Furthermore, myeloid derived suppressor cells (MDSCs) had a significant decrease in circulation and in tumor site. In brief, these findings showed menk could inhibit tumor growth in vitro and in vivo, providing direction of further research and clinical application prospect.
Journal • IO biomarker
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CASP3 (Caspase 3) • CASP8 (Caspase 8)
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BAX expression
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methionine enkephalin (STAT-401)
over3years
A novel mechanism of lung cancer inhibition by methionine enkephalin through remodeling the immune status of the tumor microenvironment. (PubMed, Int Immunopharmacol)
Immunohistochemical analysis of the expression of cytokines in the TME showed that MENK upregulated IL-15, IL-21, IFN-γ, and granzyme B and downregulated IL-10 and TGF-β1 in mice. Taken together, these finding indicate that MENK may be a potential agent for lung cancer treatment in the future, especially for overcoming immune escape and immune resistance.
Journal
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CD8 (cluster of differentiation 8) • IFNG (Interferon, gamma) • CD4 (CD4 Molecule) • IL10 (Interleukin 10) • GZMB (Granzyme B) • TGFB1 (Transforming Growth Factor Beta 1) • IL21 (Interleukin 21)
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methionine enkephalin (STAT-401)
over3years
Regulatory role of methionine enkephalin in myeloid-derived suppressor cells and macrophages in human cutaneous squamous cell carcinoma. (PubMed, Int Immunopharmacol)
Furthermore, JAK2/STAT3, an important tumor-promotion and immunosuppression signaling pathway that is involved in MDSC expansion in tumors and macrophage polarization, was inhibited. These findings highlight the potential of the JAK2/STAT3 signaling pathway as a therapeutic target and suggest the clinical application of MENK for CSCC.
Journal
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BCL2 (B-cell CLL/lymphoma 2) • CASP3 (Caspase 3)
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methionine enkephalin (STAT-401)
over3years
Methionine enkephalin (MENK) suppresses lung cancer by regulating the Bcl-2/Bax/caspase-3 signaling pathway and enhancing natural killer cell-driven tumor immunity. (PubMed, Int Immunopharmacol)
Further studies showed that MENK treatment increased the expression of natural killer (NK) cell-related cytokines such as granzyme B and interferon-γ and NK cell activation. Thus, we concluded that MENK might inhibit the proliferation of lung cancer cells by activating the Bcl-2/Bax/caspase-3 signaling pathway and enhancing immunogenicity and NK cell-driven tumor immunity.
Journal • IO biomarker
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BCL2 (B-cell CLL/lymphoma 2) • CCND1 (Cyclin D1) • CASP3 (Caspase 3) • HMGB1 (High Mobility Group Box 1) • GZMB (Granzyme B) • CALR (Calreticulin) • NKG2D (killer cell lectin like receptor K1)
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methionine enkephalin (STAT-401)