TT-1
TT-1 is an acetylcholinesterase inhibitor (human IC50 = 18.6 μM) and an amyloid β (1-42) aggregation inhibitor with antioxidant capacity, and it exerts antitumor effects by downregulating ADAM10 expression, upregulating MICA, and activating the intrinsic mitochondrial apoptosis pathway. TT-1 can be used for research on Alzheimer's disease, liver cancer, and epilepsy.
For research use only. We do not sell to patients.
- CAS No.: 1644159-87-4
- Formula: C57H108N14O14
- Molecular Weight:1213.55
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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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- References
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Help & FAQs
Biological Activity
Description
IC50 & Target
[1]|
AChE 18.6 μM (IC50) |
Cellular Effect
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Cell Line
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Type | Value | Description | References |
|---|---|---|---|---|
| HepG2 | IC50 |
3.762 μg/mL
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Inhibition of human hepatocellular carcinoma HepG-2 cell proliferation assessed by MTT assay after 72 hrs.
Inhibition of human hepatocellular carcinoma HepG-2 cell proliferation assessed by MTT assay after 72 hrs.
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28585428 |
| Huh-7 | IC50 |
5.823 μg/mL
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Inhibition of human hepatocellular carcinoma Huh7 cell proliferation assessed by MTT assay after 72 hrs.
Inhibition of human hepatocellular carcinoma Huh7 cell proliferation assessed by MTT assay after 72 hrs.
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28585428 |
In Vitro
TT-1 (6.25-50 µM; 10 min) exhibits potent AChE inhibitory activity against recombinant human AChE, with an IC50 of 18.6 µM[1].
TT-1 (20-35 ng; 5-14 days) injected into the rat motor cortex induces reciprocal changes in Zif268 and Fos-like immunoreactivity, with enhanced immunoreactivity at the epileptic focus and decreased immunoreactivity in the surrounding cortex, suggesting that the epileptic focus is in a state of functional disconnection[4].
TT-1 (10 µM) exhibits radical scavenging activity at 10 µM, with an ORAC value of 5.1 µM Trolox equivalents[1].
TT-1 (10-40 µM; 24 h) inhibits Aβ (1-42) peptide aggregation in a dose-dependent manner, reaching 100% inhibition at 20 µM and 40 µM[1].
TT-1 (0.5-32 μg/mL; 48-72 h) exhibits potent dose-dependent cytotoxicity against HepG-2 and Huh7 cells, with IC50 values of 3.762 μg/mL and 5.823 μg/mL, respectively[2].
TT-1 (0.5-2 μg/mL) treatment increases MICA expression on HepG-2 and Huh7 cells in a dose-dependent manner[2].
TT-1 (0.5-16 μg/mL; 48 h) reduces the secretion of soluble MICA from HepG-2 and Huh7 cells in a dose-dependent manner[2].
TT-1 (0.5-2 μg/mL; 48 h) downregulates ADAM 10 mRNA expression in a dose-dependent manner in HepG-2 and Huh7 cells[2].
TT-1 (0.5-2 μg/mL; 48 h) decreases ADAM 10 protein expression in HepG-2 and Huh7 cells in a dose-dependent manner[2].
TT-1 (2 μg/mL; 4 h) alone does not significantly enhance the cytotoxicity of NK92 against HepG-2 and Huh7 cells, but when combined with IFN-α, it shows enhanced cytotoxicity at E:T ratios of 10:1 and 5:1[2].
MedChemExpress (MCE) has not independently confirmed the accuracy of these methods. They are for reference only.
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Cell Line:HepG-2 and Huh7
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Concentration:0.5, 1, 2, 4, 8, 16, 32 μg/mL (48 h); 32 μg/mL (viability); IC50 at 72 h
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Incubation Time:48 h; 72 h (IC50)
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Result:Inhibited HepG-2/Huh7 cell proliferation in a dose-dependent manner.
Achieved IC50 values of 3.762 μg/mL for HepG-2 cells and 5.823 μg/mL for Huh7 cells at 72 h.
Decreased cell viability of HepG-2 and Huh7 cells to 14.8% and 26.9%, respectively, at 32 μg/mL.
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Cell Line:HepG-2 and Huh7
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Concentration:0.5, 1, 2, 4, 8, 16 μg/mL
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Incubation Time:48 h
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Result:Inhibited the expression of sMICA in a dose-dependent manner.
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Cell Line:HepG-2 and Huh7
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Concentration:0.5, 1, 2 μg/mL; 1 μg/mL (significant difference)
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Incubation Time:48 h
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Result:Dose-dependently down-regulated the mRNA level of ADAM 10 in HepG-2/Huh7 cells.
A significant difference in ADAM 10 mRNA appeared when the concentration reached 1 μg/mL.
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Cell Line:HepG-2 and Huh7
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Concentration:0.5, 1, 2 μg/mL; 0.5, 1, and 2 μg/mL
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Incubation Time:48 h
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Result:Decreased the expression of ADAM 10.
Reduced the ratio of ADAM 10 to β-actin to 0.35 at 2 μg/mL, compared to 0.46 in the group without TT-1.
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Cell Line:HepG-2 and Huh7
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Concentration:2 μg/mL
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Incubation Time:4 h
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Result:Did not cause obvious changes in NK cytotoxicity when added alone.
Achieved NK cytotoxicity of approximately 45% at the 10:1 E:T ratio and 35% at the 5:1 E:T ratio in HepG-2 cells when combined with IFN-α.
Exhibited similar results in Huh7 cells.
In Vivo
Oral administration of TT-1 (100-200 mg/kg; p.o.; once a day; 11 days) improves learning and memory functions in scopolamine-induced amnesiac mice, with the 200 mg/kg dose significantly reducing brain AChE activity and increasing reduced GSH levels[1].
Tetanus toxin (TT-1) (20-35 ng; i.c. injection into the motor cortex; single administration) injected into the rat motor cortex induces chronic focal epilepsy with a latent period of 4-13 days, producing seizure-dependent, reciprocal changes in Zif268 immunoreactivity (enhanced in a cluster at the injection site, reduced in the immediate surround) and widespread decreases in Fos-like immunoreactivity outside the injection site[4].
TT-1+IFN-α (1 mg/kg; intra-tumor; three times a week) treatment increases MICA expression on tumor cells and NKG2D expression on infiltrating NK cells in HepG-2/Huh7 xenograft tumor tissues[2].
MedChemExpress (MCE) has not independently confirmed the accuracy of these methods. They are for reference only.
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Animal Model:ICR (8-week-old, male)[1]
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Dosage:100, 200 mg/kg
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Administration:p.o. (gavage); once a day; 11 days
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Result:Prolonged step-through latency in the light box of the retention trial in the passive avoidance test.
Increased time spent in the target quadrant and higher crossing numbers in the target quadrant in the Morris water maze probe test at 200 mg/kg.
Reduced AChE activity and increased reduced GSH content in brain tissue at 200 mg/kg.
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Animal Model:BALB/c nude mice[2]
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Dosage:1 mg/kg (TT-1 alone); 1 mg/kg (TT-1) + 1 mg/kg (IFN-α) (combination)
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Administration:Intra-tumor injection; three times a week; four weeks
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Result:Inhibited tumor growth effectively as a single agent.
Enhanced antitumor activity significantly when combined with IFN-α compared to TT-1 alone.
Suppressed tumor growth inhibitory activity remarkably after NK cell depletion using anti-asialo GM-1 antibody.
Exhibited similar tumor inhibitory rate to the TT-1+IFN-α group when anti-asialo GM-1 was replaced by an isotype antibody.
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Animal Model:BALB/c nude mice[2]
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Dosage:1 mg/kg (TT-1) + 1 mg/kg (IFN-α)
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Administration:Intra-tumor injection; three times a week
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Result:Demonstrated a significant augmentation in the numbers and intensity of MICA expression in treated tumors compared to untreated groups.
Showed considerably higher expression level of NKG2D on infiltrating NK cells in tumor tissues than in tumors from untreated mice.
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Animal Model:Rats (either sex, weighing 150-290 g)[4]
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Dosage:20, 25, 35 ng
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Administration:i.c. injection into the motor cortex; single administration
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Result:Of 24 rats injected with 20 ng, 16 with 25 ng, and 7 with 35 ng, seven died of generalized seizures on postoperative day 4-11.
All remaining rats except two perfused on postoperative day 7 had seizures after a latent period of 4-13 days.
In all 7 rats in the 14-day survival group, a fan-shaped cluster of neurons showing enhanced Zif268 immunoreactivity was observed at the injection site, affecting all layers but extending mediolaterally 1.6-3.1 mm in layer II and 1.2-2.3 mm in middle layer VI.
The extent of the lightly stained zone ranged from 0.5-1.1 mm in layer II and 0.2-0.6 mm in layer VI.
In three rats that survived for 5, 7, or 14 days, a second cluster of enhanced Zif268 immunoreactive neurons was found in layer II and upper layer III of the ipsilateral rostral forelimb motor area.
Rats that survived for 14 days showed a cluster of moderately Fos-immunoreactive neurons at the injection site, especially in cortical layers III and VI.
Chemical Information
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CAS No. 1644159-87-4
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Molecular Weight 1213.55
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Formula C57H108N14O14
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SMILES
O=C(N[C@@H]([C@@H](C)CC)C(N[C@@H](CCCCN)C(N[C@@H](C)C(N[C@@H](C(C)C)C(N[C@@H](CC(C)C)C(N[C@@H](CCCCN)C(N[C@@H](C(C)C)C(N[C@@H](CC(C)C)C(N[C@@H]([C@H](O)C)C(N[C@@H]([C@H](O)C)C(O)=O)=O)=O)=O)=O)=O)=O)=O)=O)=O)[C@H](CCCCN)N
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Sequence
Lys-Ile-Lys-Ala-Val-Leu-Lys-Val-Leu-Thr-Thr
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Sequence Shortening
KIKAVLKVLTT
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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
Calculators
Concentration (start) × Volume (start) = Concentration (final) × Volume (final)
TT-1 Related Classifications
HY-P12277 Related Classifications
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