2. NF-κB Apoptosis Cytoskeleton
  3. NF-κB Apoptosis Cadherin Caspase Bcl-2 Family
  4. TKL002

TKL002 is a blood-brain barrier-permeable inhibitor of the CTH/H2S/NF-κB/EMT signaling axis. TKL002 induces G2/M phase cell cycle arrest and apoptosis in glioblastoma cells. TKL002 inhibits the migration and invasion of glioblastoma cells by upregulating E-cadherin and downregulating N-cadherin and vimentin. TKL002 is applicable to relevant research on glioblastoma.

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TKL002

TKL002 Chemical Structure

CAS No. : 3098518-95-4

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TKL002 Related Antibodies

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Description

TKL002 is a blood-brain barrier-permeable inhibitor of the CTH/H2S/NF-κB/EMT signaling axis. TKL002 induces G2/M phase cell cycle arrest and apoptosis in glioblastoma cells. TKL002 inhibits the migration and invasion of glioblastoma cells by upregulating E-cadherin and downregulating N-cadherin and vimentin. TKL002 is applicable to relevant research on glioblastoma[1].

IC50 & Target[1]

NF-κB

 

Caspase 3

 

Bax

 

Bcl-2

 

In Vitro

TKL002 (0.625-10 μmol/L; 24-72 h) potently inhibits the proliferation of U87MG, U118MG, and U251MG glioblastoma cells in a dose- and time-dependent manner with selectivity over normal LX2 cells, exhibiting IC50 values ranging from 4.141 to 6.506 μmol/L across cell lines and time points[1].
TKL002 (6 μmol/L; 48 h) induces late apoptosis in U87MG glioblastoma cells, mediated via upregulation of Bax and caspase-3 and downregulation of Bcl-2 and active-caspase-3[1].
TKL002 (2-6 μmol/L; 24 h) induces G2/M phase cell cycle arrest in U87MG and U118MG glioblastoma cells in a concentration-dependent manner, with maximum G2/M fractions of 22.68% and 30.31% at 6 μmol/L respectively[1].
TKL002 (2-6 μmol/L; 48 h) reduces CTH, cysteine, and H2S levels, increases GSH levels, and inhibits NF-κB signaling and pro-inflammatory cytokine expression in U87MG and U118MG glioblastoma cells in vitro in a dose-dependent manner[1].
TKL002 (2-6 μmol/L; 48 h) inhibits migration and invasion of U87MG and U118MG glioblastoma cells in a dose-dependent manner, mediated via upregulation of E-cadherin and downregulation of N-cadherin and vimentin to suppress epithelial-mesenchymal transition[1].

MedChemExpress (MCE) has not independently confirmed the accuracy of these methods. They are for reference only.

TKL002 Related Antibodies

Apoptosis Analysis[1]

Cell Line: U87MG
Concentration: 2, 4, 6 μM
Incubation Time: 48 h
Result: Increased late apoptosis to 22.63%.

Cell Cycle Analysis[1]

Cell Line: U87MG, U118MG glioblastoma cells
Concentration: 2, 4, 6 μM
Incubation Time: 24 h
Result: Increased the G2/M phase fraction in a concentration-dependent manner.

Cell Migration Assay [1]

Cell Line: U87MG, U118MG glioblastoma cells
Concentration: 2, 4, 6 μM
Incubation Time: 48 h
Result: Inhibited GBM cell migration.

Cell Invasion Assay[1]

Cell Line: U87MG, U118MG glioblastoma cells
Concentration: 2, 4, 6 μM
Incubation Time: 48 h
Result: Inhibited GBM cell invasion.
In Vivo

TKL002 (5-20 mg/kg; i.p.; once every other day, 7 total administrations) inhibits the growth of subcutaneous glioblastoma xenografts in a dose-dependent manner[1].
TKL002 (10-20 mg/kg; i.v., once every three days for a total of 5 administrations) can cross the blood-brain barrier, inhibit the growth of orthotopic glioblastoma in a dose-dependent manner, reduce tumor burden, maintain the physical condition of mice, and cause no obvious organ toxicity[1].

MedChemExpress (MCE) has not independently confirmed the accuracy of these methods. They are for reference only.

Animal Model: BALB/c nude (male, 4−5 weeks old, 16−18 g, subcutaneous xenograft model)[1]
Dosage: 5 mg/kg; 20 mg/kg
Administration: i.p.; every other day; 7 total doses
Result: Reduced mean subcutaneous tumor weight to 1.117 g (5 mg/kg) and 0.530 g, compared to 1.458 g in vehicle control.
Achieved similar tumor weight and volume reduction as 5 mg/kg temozolomide at 20 mg/kg.
Showed dose-dependent reductions in splenic index.
Caused minimal pathological changes in liver, spleen, and kidney; no significant changes in heart, liver, lung, or kidney indices.
Animal Model: BALB/c nude (male, 4−5 weeks old, 16−18 g, orthotopic xenograft model)[1]
Dosage: 10 mg/kg; 20 mg/kg
Administration: i.v. via tail vein; every 3 days; 5 total doses
Result: Reduced in vivo bioluminescent signal intensity to 13.62×104 photons/s (10 mg/kg) and 8.52×104 photons/s (20 mg/kg) on days 15 and 20, versus 25.21×104 photons/s in vehicle control.
Reduced ex vivo tumor bioluminescent signal intensity to 21.48×104 photons/s (10 mg/kg) and 9.20×104 photons/s (20 mg/kg), versus 63.88×104 photons/s in controls.
Maintained normal body condition in 20 mg/kg group, while control mice exhibited weight loss, reduced activity, and cachexia.
Showed marked, dose-dependent reductions in CTH-positive tumor area, with the 20 mg/kg group showing the most pronounced decrease.
Showed a higher survival rate in the 20 mg/kg group, though the difference was not statistically significant.
Caused no significant differences in organ indices among groups.
Molecular Weight

420.40

Formula

C21H20F4N4O
CAS No.
SMILES

COC1=CC=C(C2=C1)N=C(C=C2C(F)(F)F)NC3=CC=C(C(F)=C3)N4CCNCC4
Shipping

Room temperature in continental US; may vary elsewhere.
Storage

Please store the product under the recommended conditions in the Certificate of Analysis.
Purity & Documentation
References
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TKL002 Related Classifications

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Help & FAQs
  • Do most proteins show cross-species activity?

    Species cross-reactivity must be investigated individually for each product. Many human cytokines will produce a nice response in mouse cell lines, and many mouse proteins will show activity on human cells. Other proteins may have a lower specific activity when used in the opposite species.

Keywords:

TKL0023098518-95-4TKL 002TKL-002NF-κBApoptosisCadherinCaspaseBcl-2 FamilyNuclear factor-κBNuclear factor-kappaBU118MGCystathionine γ-lyase (CTH)U251MGglioblastomapro-inflammatory cytokineU87MGG2/M cell cycle arresthydrogen sulfideapoptosisInhibitorinhibitorinhibit

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