Tertomotide hydrochloride
Tertomotide hydrochloride (GV-1001 hydrochloride) is a 16-amino acid peptide derived from hTERT, with both cell-penetrating and immunostimulatory activities, and it can cross the blood-brain barrier. Tertomotide hydrochloride binds to STING, HO-1, eHSP70, eHSP90, bradykinin receptor 1, VEGFR-2, NF-κB, p38 MAPK and Smad2. Tertomotide hydrochloride induces type I interferon production, mitochondrial DNA stress and T-cell responses; inhibits HBV replication, angiogenesis, TGF-β signaling pathway, NF-κB activation, endothelial-mesenchymal transition (EndMT) and fibrosis; regulates microglia; and exerts neuroprotective, anti-inflammatory, antioxidant, anti-apoptotic and anti-tumor effects. Tertomotide hydrochloride can be used in research related to hepatitis B virus infection, Alzheimer's disease, non-small cell lung cancer, atherosclerosis and depression.
For research use only. We do not sell to patients.
- CAS No.: 922174-60-5
- Formula: C85H147ClN26O21
- Molecular Weight:1904.69
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Storage:
Please store the product under the recommended conditions in the Certificate of Analysis.
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Biological Activity
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Chemical Information
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Biological Activity
Description
Cellular Effect
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Cell Line
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Type | Value | Description | References |
|---|---|---|---|---|
| HepG2 | IC50 |
0.67 μM
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Inhibition of extracellular HBV virion production in HBV-transfected HepG2 cells incubated for 48 h, with supernatants collected for extracellular HBV virion DNA analysis and cell viability assessed via MTS assay.
Inhibition of extracellular HBV virion production in HBV-transfected HepG2 cells incubated for 48 h, with supernatants collected for extracellular HBV virion DNA analysis and cell viability assessed via MTS assay.
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32508804 |
In Vitro
Tertomotide (0.01-10 μM; 48 h) hydrochloride (GV-1001 (hydrochloride)) potently inhibits HBV replication in HBV-transfected HepG2 cells with an IC50 of 0.67 μM and no detectable cytotoxicity[1].
Tertomotide (1-10 μM; 48 h) hydrochloride reduces HBV virion production in stable HepG2-2.15 cells in a dose-dependent manner with no detectable cytotoxicity[1].
Tertomotide hydrochloride inhibits HBV cccDNA formation, pgRNA transcription, and nucleocapsid assembly in HBV-transfected HepG2 cells[1].
Tertomotide (10 μM; 24-48 h) hydrochloride exerts synergistic anti-HBV effects with Lamivudine (HY-B0250) and Entecavir (HY-13623) in stable HepG2-2.15 cells[1].
Tertomotide (10 μM; 24 h) hydrochloride has an anti-HBV effect in HepG2-2.15 cells that is dependent on interactions with extracellular HSP70 and HSP90[1].
Tertomotide (10 μM; 12 h) hydrochloride requires phagosomal escape and cytosolic localization for its IFN-I-mediated anti-HBV effect in HepG2-2.15 cells[1].
Tertomotide (10-20 μM; 24-48 h) hydrochloride induces IFN-I production in HepG2-2.15 cells via activation of the IRF3-STAT1 signaling axis[1].
Tertomotide (100 μM; 1 h pre-treatment + 48 h incubation) hydrochloride suppresses ENO1-induced production of TNF−α, IL-1β, and IL-6 in healthy volunteer-derived Con A-activated PBMCs[5].
Tertomotide (2.5-10 μM; 12-48 h) hydrochloride induces mitochondrial DNA stress in HepG2-2.15 cells, which drives IFN-I-mediated anti-HBV activity[1].
Tertomotide (10 µg/mL; 48 h) hydrochloride mitigates Doxorubicin-induced oxidative stress by reducing mitochondrial and cytoplasmic ROS accumulation and restoring cellular ATP levels in human umbilical vein endothelial cells[4].
Tertomotide (1 nM-10 μM; 24-48 h) hydrochloride has an anti-HBV effect in HBV-transfected HepG2 cells that is dependent on enhanced HO-1 expression[1].
Tertomotide (24 h) hydrochloride enhances migration of primary mouse microglia[2].
Tertomotide hydrochloride induces lamellipodium formation in primary mouse microglia, promoting a migratory cell phenotype[2].
Tertomotide (2-10 µg/mL; 48 h) hydrochloride suppresses Doxorubicin-induced NF-κB activation by inhibiting p65 phosphorylation and nuclear translocation in human umbilical vein endothelial cells[4].
Tertomotide (100 μM; 1 h pre-treatment) hydrochloride suppresses ENO1-induced activation of p38 MAPK and NF-κB in healthy volunteer-derived Con A-activated PBMCs[5].
Tertomotide (0.05-5 μM; 30 min pre-incubation, followed by 30 min VEGF-A stimulation) hydrochloride dose-dependently inhibits VEGF-A-stimulated permeability in HUVECs by suppressing VE-cadherin phosphorylation and stabilizing VE-cadherin at cell-cell contacts[3].
Tertomotide (0.05-5 μM; 30 min pre-incubation, followed by 16 h VEGF-A stimulation) hydrochloride dose-dependently inhibits VEGF-A-stimulated migration in HUVECs, an effect independent of its anti-proliferative activity[3].
Tertomotide (5 μM; 30 min pre-incubation, followed by 18 h VEGF-A stimulation for invasion assay; 30 min pre-incubation, followed by 16 h VEGF-A stimulation for zymography and RT-PCR) hydrochloride inhibits VEGF-A-stimulated invasion in HUVECs, at least in part by reducing MMP-2 activity and expression, and also inhibits FGF-2-stimulated invasion[3].
Tertomotide (0.05-5 μM; 30 min pre-incubation, followed by 6 h VEGF-A stimulation) hydrochloride dose-dependently inhibits VEGF-A-stimulated tube formation in HUVECs, and also inhibits FGF-2-stimulated tube formation[3].
Tertomotide (5 μM; 30 min pre-incubation, followed by 5 min, 15 min, or 24 h VEGF-A stimulation) hydrochloride inhibits VEGF-A/VEGFR-2 signaling in HUVECs by blocking VEGFR-2 phosphorylation and downstream activation of FAK, Src, MEK, ERK, and Akt, and by reducing VEGFR-2 expression; it also inhibits FGF-2-stimulated Src and ERK phosphorylation[3].
Tertomotide (0.05-5 μM; 30 min pre-incubation, followed by 24 h VEGF-A stimulation) hydrochloride dose-dependently inhibits VEGF-A-stimulated proliferation in HUVECs via G1 cell cycle arrest without reducing cell viability, and also inhibits FGF-2-stimulated proliferation[3].
Tertomotide (0.05-5 μM; 30 min pre-incubation, followed by 24 h or 18 h 10% FBS stimulation) hydrochloride dose-dependently inhibits 10% FBS-stimulated proliferation and invasion in A549 and H1299 NSCLC cells, with greater potency in p53 wild-type A549 cells[3].
Tertomotide (10 µg/mL; 24-48 h) hydrochloride suppresses Doxorubicin (HY-15142A)-induced endothelial-to-mesenchymal transition and migration in human umbilical vein endothelial cells[4].
Tertomotide (1 µM; 10 days) hydrochloride suppresses ionizing radiation-induced genotoxicity and modulates proliferation and senescence-related protein expression in primary normal human oral keratinocytes[6].
Tertomotide (1 µM; 10 days) hydrochloride suppresses ionizing radiation-induced TGF-β signaling and epithelial-mesenchymal transition in primary normal human oral keratinocytes[6].
Tertomotide (1 µM; 24 h-10 days) hydrochloride suppresses TGF-β-induced epithelial-mesenchymal transition in primary normal human oral keratinocytes and TGF-β-enhanced migration in SCC 4 squamous cell carcinoma cells[6].
Tertomotide (1 µM; 10 days) hydrochloride inhibits TGF-β-induced target gene expression and Smad2 binding to collagen gene promoters in primary normal human oral fibroblasts[6].
Tertomotide (1-8 µM; 10 days) hydrochloride inhibits TGF-β-induced myofibroblast differentiation and TGF-β signaling in primary normal human oral fibroblasts[6].
Tertomotide (5 μM; 30 min pre-incubation, followed by 48 h 10% FBS stimulation) hydrochloride inhibits 10% FBS-induced VEGF expression and secretion in p53 wild-type A549 NSCLC cells, but not in p53-deficient H1299 cells[3].
Tertomotide (2-10 µg/mL) hydrochloride suppresses Doxorubicin-induced overexpression of proinflammatory cytokines and TGF-β/Smad pathway genes in human umbilical vein endothelial cells[4].
Tertomotide (10 µg/mL; 48 h) hydrochloride prevents Doxorubicin-induced mitochondrial structural damage, ferrous iron accumulation, and lipid peroxidation in human umbilical vein endothelial cells[4].
Tertomotide (100 μM; 1 h) hydrochloride does not affect Con A (Concanavalin A) (HY-P2149)-induced ENO1 surface expression on healthy volunteer-derived Con A-activated PBMCs[5].
Tertomotide (1-200 μM; 48 h) hydrochloride has no effect on the viability or proliferation of unstressed rat embryonic neural stem cells at concentrations up to 100 μM, but restores viability and proliferation in a concentration-dependent manner in rat embryonic neural stem cells injured by 20 μM Aβ25-35 (β-Amyloid (25-35)) (HY-P0128) oligomer[9].
Tertomotide (1-100 μM; 48 h) hydrochloride inhibits apoptosis in a concentration-dependent manner in rat embryonic neural stem cells injured by 20 μM Aβ25-35 oligomer[9].
Tertomotide (1-50 μM; 24 h) hydrochloride restores migratory capacity in rat embryonic neural stem cells injured by 20 μM Aβ25-35 oligomer[9].
Tertomotide (1-100 μM; 48 h) hydrochloride protects primary rat cortical neurons from 20 μM Aβ25-35-induced toxicity, with a weaker effect than seen in rat embryonic neural stem cells[9].
Tertomotide (1-10 μM; 4-8 h) hydrochloride accumulates in the cytoplasm and mitochondria of unstressed rat embryonic neural stem cells in a time-dependent manner, and translocates to the nucleus in rat embryonic neural stem cells injured by 20 μM Aβ25-35 oligomer[9].
Tertomotide (1-50 μM; 48 h) hydrochloride reduces reactive oxygen species production in a concentration-dependent manner in rat embryonic neural stem cells injured by 20 μM Aβ25-35 oligomer, without directly scavenging ROS in a cell-free environment[9].
Tertomotide (1-50 μM; 48 h) hydrochloride reduces oxidative mitochondrial DNA damage in a concentration-dependent manner in rat embryonic neural stem cells injured by 20 μM Aβ25-35 oligomer[9].
Tertomotide (1-50 μM; 48 h) hydrochloride restores mitochondrial membrane potential and ATP levels in a concentration-dependent manner in rat embryonic neural stem cells injured by 20 μM Aβ25-35 oligomer[9].
Tertomotide (1-100 μM; 48 h) hydrochloride restores the expression of survival-related proteins and reduces the expression of death-related proteins in a concentration-dependent manner in rat embryonic neural stem cells injured by 20 μM Aβ25-35 oligomer[9].
The protective effect of Tertomotide (10 μM; 48 h) against 20 μM Aβ25-35 oligomer in rat embryonic neural stem cells is partially mediated by the PI3K pathway[9].
Tertomotide (1 μM) hydrochloride restores the normal differentiation balance of rat embryonic neural stem cells injured by 20 μM Aβ25-35 oligomer, promoting neuronal differentiation and reducing astrocytic differentiation, without affecting differentiation under unstressed conditions[9].
Tertomotide (1 µM; 7-14 days) hydrochloride attenuates ionizing radiation-induced premature senescence and restores proliferation and colony formation in primary normal human oral keratinocytes[6].
MedChemExpress (MCE) has not independently confirmed the accuracy of these methods. They are for reference only.
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Cell Line:human umbilical vein endothelial cells (HUVECs)
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Concentration:0.05 μM; 0.5 μM; 5 μM
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Incubation Time:30 min pre-incubation, followed by 24 h VEGF-A stimulation
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Result:Dose-dependently inhibited VEGF-A-stimulated HUVEC proliferation.
Showed no effect on cell viability at the highest tested concentration.
Induced G1 cell cycle arrest by suppressing VEGF-A-induced phosphorylation of pRb, down-regulating cyclin-dependent kinase 4 (Cdk4) and cyclin E, and up-regulating p27^Kip1.
Inhibited FGF-2-stimulated HUVEC proliferation similarly to VEGF-A-stimulated cells.
Had no effect on basal HUVEC proliferation when used alone.
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Cell Line:human umbilical vein endothelial cells (HUVECs)
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Concentration:0.05-5 μM; 5 μM (in presence of mitomycin C)
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Incubation Time:30 min pre-incubation, followed by 16 h VEGF-A stimulation
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Result:Dose-dependently inhibited VEGF-A-stimulated HUVEC migration.
Pre-treatment with mitomycin C to block cell proliferation did not alter the anti-migratory effect, demonstrating the activity is independent of proliferation inhibition.
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Cell Line:human umbilical vein endothelial cells (HUVECs)
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Concentration:5 μM
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Incubation Time:30 min pre-incubation, followed by 18 h VEGF-A stimulation (invasion assay); 30 min pre-incubation, followed by 16 h VEGF-A stimulation (zymography and RT-PCR)
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Result:Inhibited VEGF-A-stimulated HUVEC invasion.
Reduced VEGF-A-induced MMP-2 activity.
Suppressed VEGF-A-induced MMP-2 expression to near unstimulated control levels.
Inhibited FGF-2-stimulated HUVEC invasion.
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Cell Line:human umbilical vein endothelial cells (HUVECs)
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Concentration:5 μM
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Incubation Time:30 min pre-incubation, followed by 5 min VEGF-A stimulation (VEGFR-2, FAK, Src, MEK phosphorylation analysis); 30 min pre-incubation, followed by 15 min VEGF-A stimulation (ERK, Akt, p70^S6K phosphorylation analysis); 30 min pre-incubation, followed by 24 h VEGF-A stimulation (VEGFR-2 protein and mRNA expression analysis)
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Result:Abrogated VEGF-A-induced phosphorylation of VEGFR-2 on total tyrosine residues and the Y1175 residue.
Blocked VEGF-A-induced phosphorylation of downstream signaling components FAK (Y397), Src (Y416), MEK, ERK, and Akt, but did not affect p70^S6K phosphorylation.
Suppressed VEGF-A-induced increases in VEGFR-2 protein and mRNA expression, restoring levels to near unstimulated control values.
Inhibited FGF-2-stimulated phosphorylation of Src and ERK.
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Cell Line:human non-small cell lung cancer (NSCLC) cells (A549, H1299)
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Concentration:0.05 μM; 0.5 μM; 5 μM
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Incubation Time:30 min pre-incubation, followed by 24 h 10% FBS stimulation (proliferation); 30 min pre-incubation, followed by 18 h 10% FBS stimulation (invasion)
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Result:Dose-dependently inhibited 10% FBS-stimulated proliferation of both A549 (p53 wild-type) and H1299 (p53-deficient) NSCLC cells, with A549 cells showing greater sensitivity.
Inhibited 10% FBS-stimulated invasion of both cell lines, with more potent effects observed in A549 cells.
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Cell Line:human non-small cell lung cancer (NSCLC) cells (A549)
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Concentration:5 μM
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Incubation Time:30 min pre-incubation, followed by 48 h 10% FBS stimulation
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Result:Suppressed 10% FBS-induced VEGF expression and secretion in A549 cells.
Showed no effect on VEGF expression or secretion in H1299 cells.
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Cell Line:human umbilical vein endothelial cells (HUVECs)
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Concentration:10 µg/mL
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Incubation Time:48 h
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Result:Mitigated Doxorubicin-induced mitochondrial fragmentation (shortened, rounded morphology).
Entirely prevented Doxorubicin-induced increases in mitochondrial ferrous iron levels and lipid peroxidation.
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Cell Line:primary normal human oral keratinocytes (NHOKs)
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Concentration:1 µM
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Incubation Time:7 days (proliferation kinetics); 10-14 days (SA β-Gal staining, colony formation)
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Result:Reduced IR-induced senescent cellular morphology in NHOKs exposed to 6 Gy IR.
Mitigated IR-induced proliferation arrest, showing increased cell numbers over 7 days compared to irradiated control cells.
Significantly reduced the percentage of SA β-Gal-positive cells across tested IR doses (2, 4, 6, 8, 10 Gy).
Restored colony forming ability in irradiated NHOKs, with higher colony counts observed across all tested IR doses compared to irradiated control cells.
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Cell Line:primary normal human oral keratinocytes (NHOKs)
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Concentration:1 µM
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Incubation Time:10 days post-6 Gy IR exposure
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Result:Increased the level of Grainyhead-like 2 (GRHL2) and phosphorylated Akt (Ser473), and decreased the levels of N-Cadherin, phosphorylated p53 (Ser15), and p21/WAF1 in irradiated NHOKs.
Reduced the percentage of cells with >3 intranuclear 53BP1 and γ-H2AX foci, indicating enhanced DNA DSB repair.\nDecreased the levels of phosphorylated Smad2/3, Smad4, and TGF-β target mesenchymal markers including ZEB1, fibronectin (FN), N-Cadherin, and Snail in irradiated NHOKs, reducing the IR-induced mesenchymal phenotype.
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Cell Line:primary normal human oral fibroblasts (NHOFs)
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Concentration:1 µM
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Incubation Time:10 days with TGF-β exposure
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Result:Suppressed TGF-β-induced increases in mRNA levels of Col1a1, Col3a1, FN, N-Cadherin, ZEB1, and ZEB2 in NHOFs.
Markedly reduced Smad2 binding to the -1750 bp, -1000 bp, and -200 bp regions of the Col1a1 promoter, and to the Col3a1 promoter in TGF-β-treated NHOFs.
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Cell Line:primary normal human oral fibroblasts (NHOFs)
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Concentration:1 µM; 2 µM; 4 µM; 6 µM; 8 µM
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Incubation Time:10 days with TGF-β exposure
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Result:Reduced TGF-β-induced increases in α-SMA, Snail, FN, N-Cadherin, Col1a1, Col3a1, and phosphorylated Smad2 in NHOFs, with effects observed across all tested concentrations.
Suppressed TGF-β-induced increases in α-SMA and ZEB1 protein levels as detected by immunofluorescence staining.
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Cell Line:rat embryonic neural stem cells (NSCs)
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Concentration:1 μM, 10 μM, 50 μM, 100 μM, 200 μM (48 h incubation alone); 1 μM, 10 μM, 50 μM, 100 μM (48 h simultaneous incubation with 20 μM Aβ25-35)
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Incubation Time:48 h (alone or with Aβ25-35); 5 h (BrdU-labeling for proliferation assessment)
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Result:Showed no effect on rat NSC viability or proliferation at concentrations up to 100 μM when used alone.
Restored Aβ-induced reductions in NSC viability and proliferation in a concentration-dependent manner when co-treated with 20 μM Aβ25-35.
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Cell Line:rat embryonic neural stem cells (NSCs)
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Concentration:1 μM, 10 μM, 50 μM, 100 μM (48 h simultaneous incubation with 20 μM Aβ25-35)
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Incubation Time:48 h
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Result:Significantly reduced the number of apoptotic cells in a concentration-dependent manner when co-treated with 20 μM Aβ25-35, counteracting the increased apoptosis caused by Aβ25-35 alone.
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Cell Line:rat embryonic neural stem cells (NSCs)
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Concentration:1 μM, 10 μM, 50 μM (24 h incubation with 20 μM Aβ25-35)
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Incubation Time:24 h
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Result:Effectively restored migratory activity of rat NSCs when co-treated with 20 μM Aβ25-35, counteracting the reduced migratory capacity caused by Aβ25-35 alone.
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Cell Line:primary rat cortical neurons (7 days in vitro)
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Concentration:1 μM, 10 μM, 50 μM, 100 μM (48 h simultaneous incubation with 20 μM Aβ25-35)
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Incubation Time:48 h
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Result:Protected primary rat cortical neurons from Aβ-induced toxicity when co-treated with 20 μM Aβ25-35, with a weaker protective effect than that observed in rat NSCs.
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Cell Line:rat embryonic neural stem cells (NSCs)
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Concentration:1 μM, 10 μM, 50 μM (48 h simultaneous incubation with 20 μM Aβ25-35)
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Incubation Time:48 h
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Result:Effectively decreased oxidative mitochondrial DNA damage in a concentration-dependent manner when co-treated with 20 μM Aβ25-35, counteracting the increased damage caused by Aβ25-35 alone.
In Vivo
Tertomotide (1 mg/kg; s.c.; three times a week; 8 weeks) hydrochloride rescues memory deficits and synaptic loss, reduces Aβ plaque burden and neuroinflammation, and promotes microglial migration and phagocytosis toward large Aβ plaques in 5xFAD mice by modulating microglial phenotypes toward homeostatic and phagocytic DAM2 states[2].
Tertomotide (hydrochloride) crosses the intact blood-brain barrier in wild-type mice[2].
Tertomotide (1-5 mg/kg; s.c.; daily; 4 weeks) hydrochloride exerts antifibrotic activity in Bleomycin (HY-108345)-induced dermal fibrosis in female C57BL/6 mice, reducing dermal thickness and Col3a1 deposition[6].
Tertomotide (0.2-5 mg/kg; s.c.; daily; 7 days) hydrochloride exerts antidepressant effects in a mouse chronic restraint stress model, with 1 mg/kg and 5 mg/kg doses reversing depressive-like behaviors, 1 mg/kg normalizing anxiety-like behaviors and cognitive deficits, and tested doses modulating hypothalamic-pituitary-adrenal axis activity by reducing serum corticosterone levels and suppressing hypothalamic neuron activation[12].
Tertomotide (1 mg/kg; s.c.; daily; 7 days) hydrochloride suppresses acute stress-induced serum corticosterone elevation in mice, indicating modulation of hypothalamic-pituitary-adrenal axis activity[12].
Tertomotide (2 mg/kg; i.p.; three times per week; 9 weeks) hydrochloride prevents Doxorubicin-induced systemic and vascular inflammation, lipid accumulation, and monocyte/macrophage infiltration in arterial walls, thereby inhibiting atherosclerosis development in high-fat diet-fed ApoE-deficient mice[4].
MedChemExpress (MCE) has not independently confirmed the accuracy of these methods. They are for reference only.
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Animal Model:C57BL/6N transgenic (female, age-matched)[1]
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Dosage:50 µg/kg
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Administration:i.v.; twice weekly; 8 weeks
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Result:Showed no significant reduction in serum HBsAg or extracellular HBV virion levels after 4 weeks compared to PBS controls.
Reduced serum HBV virion levels significantly after 8 weeks compared to PBS controls.
Produced a 20% mean reduction in serum HBsAg levels after 8 weeks compared to PBS controls.
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Animal Model:Heterozygous 5xFAD (male, 6-7-month-old, Alzheimer's disease model); C57BL/6 wild-type littermates[2]
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Dosage:1 mg/kg
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Administration:s.c.; three times a week; 8 weeks
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Result:Improved recognition memory in the novel object recognition test.
Recovered spatial memory deficits in the Y-maze spontaneous alternation assay.
Rescued hippocampal CA1 neuron spine density.
Increased postsynaptic density protein 95 (PSD95) levels in the hippocampus.
Reduced amyloid β (Aβ) plaque intensity in the hippocampus and cortex.
Decreased average Aβ plaque diameter.
Increased the number of CD68-positive phagocytic microglia and total microglia per Aβ plaque, particularly around large plaques (diameter > 45 μm).
Increased the proportion of homeostatic and stage II disease-associated microglia (DAM2) populations.
Upregulated DAM2 genes associated with phagocytic activity (Trem2, Tyrobp, Ctsl) and cell migration.
Elevated gene module scores for migration and phagocytosis in DAM2 microglia.
Decreased neuroinflammation as measured by reduced IBA1 and GFAP intensities, and downregulated transcript levels of Il1b, Il6, Tnf, and Cxcl1 in the hippocampus and cortex.
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Animal Model:C57BL/6 background (8-week-old male, Apolipoprotein E-deficient, maintained on high-fat diet, challenged with Doxorubicin)[4]
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Dosage:2 mg/kg
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Administration:i.p.; three times per week; 9 weeks
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Result:Mitigated Doxorubicin-induced increases in serum levels of proinflammatory cytokines (IL-6, IL-8, TNF-α, IL-1β).
Reversed Doxorubicin-induced upregulation of TNF-α, IL-1β, and IL-6 mRNA expression in arterial tissue.
Completely prevented Doxorubicin-induced increases in arterial wall lipid deposition (as measured by Oil Red O staining of en face aorta and aortic root sections).
Reduced Doxorubicin-induced macrophage/monocyte infiltration into the arterial wall.
Reversed Doxorubicin-induced p-p65 nuclear translocation and TNF-α expression in splenic cells.
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Animal Model:C57BL/6 (female, 6-week-old, Bleomycin-induced dermal fibrosis)[6]
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Dosage:1 mg/kg; 5 mg/kg
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Administration:s.c.; daily; 4 weeks
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Result:Reduced Bleomycin-induced dermal thickness.
Reduced dermal deposition of collagen type III α1 chain (Col3a1).
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Animal Model:C57BL/6 J (8-week-old male, chronic restraint stress model)[12]
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Dosage:0.2 mg/kg; 1 mg/kg; 5 mg/kg
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Administration:s.c.; daily; 7 days
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Result:Reversed stress-induced reductions in sucrose preference at 1 mg/kg and 5 mg/kg doses.
Decreased stress-increased immobility time in the tail suspension test at 1 mg/kg and 5 mg/kg doses.
Normalized stress-reduced time spent in the center zone of the open field test at 1 mg/kg dose.
Improved stress-impaired spatial working memory in the Y-maze test at 1 mg/kg dose.
Showed a trend toward restoring stress-reduced nest-building activity at 1 mg/kg dose.
Suppressed stress-induced activation of c-fos-positive corticotropin-releasing hormone neurons in the hypothalamic paraventricular nucleus at 1 mg/kg dose.
Reduced stress-elevated serum corticosterone levels to near control group levels at 1 mg/kg dose.
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Animal Model:C57BL/6 J (8-week-old male, acute restraint stress model)[12]
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Dosage:1 mg/kg
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Administration:s.c.; daily; 7 days
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Result:Reduced stress-elevated serum corticosterone levels to near those observed in the control group.
Chemical Information
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CAS No. 922174-60-5
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Molecular Weight 1904.69
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Formula C85H147ClN26O21
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Synonyms
GV-1001 hydrochloride
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Sequence
Glu-Ala-Arg-Pro-Ala-Leu-Leu-Thr-Ser-Arg-Leu-Arg-Phe-Ile-Pro-Lys
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Sequence Shortening
EARPALLTSRLRFIPK
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Shipping
Room temperature in continental US; may vary elsewhere.
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Storage
Please store the product under the recommended conditions in the Certificate of Analysis.
Purity & Documentation
References
[7]. Koh SH, et al. Efficacy and safety of GV1001 in patients with moderate-to-severe Alzheimer's disease already receiving donepezil: a phase 2 randomized, double-blind, placebo-controlled, multicenter clinical trial. Alzheimer's research & therapy. 2021 Mar 26;13(1):66. [Content Brief]
[8]. Kyte JA, et al. Cancer vaccination with telomerase peptide GV1001. Expert opinion on investigational drugs. 2009 May;18(5):687-94. [Content Brief]
[9]. Park HH, et al. Novel vaccine peptide GV1001 effectively blocks β-amyloid toxicity by mimicking the extra-telomeric functions of human telomerase reverse transcriptase. Neurobiology of aging. 2014 Jun;35(6):1255-74. [Content Brief]
Calculators
Concentration (start) × Volume (start) = Concentration (final) × Volume (final)
Tertomotide hydrochloride Related Classifications
HY-105067A Related Classifications
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