BCI (Synonyms: (E)-BCI) |
| Katalog-Nr.GC38646 |
BCI, als selektiver Dual-spezifischer Phosphatase-6 (DUSP6)-Inhibitor, kann das Tumorwachstum und die Entzündung von Makrophagen hemmen.
Products are for research use only. Not for human use. We do not sell to patients.
Cas No.: 1245792-51-1
Sample solution is provided at 25 µL, 10mM.
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BCI, als selektiver Dual-spezifischer Phosphatase-6 (DUSP6)-Inhibitor, kann das Tumorwachstum und die Entzündung von Makrophagen hemmen.[1].
In vitro zeigte BCI bei niedrigen Dosen von ≤2 μM und ≤4 μM keine zytotoxischen Effekte auf RAW264.7-Zellen bzw. BMMs. Und bei Konzentrationen von ≤4 μM hatte BCI keinen offensichtlichen Einfluss auf den Zellzyklus oder die Apoptose in BMMs.[1] In in vitro Experimenten wurde gezeigt, dass die Behandlung mit 1 μM BCI die Osteoklastogenese durch Hemmung von DUSP6 verstärkte. Darüber hinaus erhöhte BCI die Expression von osteoklastenbezogenen Genen wie NFATC1, C-fos, ACP5 und DC-STAMP.[2] In in vitro Wirksamkeitstests wurde gezeigt, dass die Behandlung mit 4 μM BCI den Anteil an Zellen, die gespaltenes Caspase-3 exprimieren, deutlich erhöhte, und 4 μM BCI verursachte bereits eine umfangreiche Zytotoxizität in KELLY- und IMR-32-Zellen, wobei nur eine Minderheit der LAN-1- und SK-N-AS-Zellen überlebte.[3] In vitro beeinflusste 1 μM BCI nicht die Gesamt-NCC- und NCC-Oberflächenexpression sowie die ERK1/2-Phosphorylierung. Die Behandlung mit 5 μM BCI kann die ERK1/2-Phosphorylierung deutlich erhöhen und die Gesamt-NCC- und NCC-Oberflächenexpression verringern.[5]
In vivo wurden Mäuse fünf aufeinanderfolgende Tage pro Woche mit 10 mg/kg BCI intraperitoneal behandelt, was die AKT-Aktivierung unterdrückte und die Tumorbildung verhinderte.[4] In in vivo Tests wurde gezeigt, dass die Behandlung mit 50, 100 und 200 mg/kg BCI oral im CPDM-Tiermodell die Anzahl der pNrf2-positiven Zellen im parodontalen Gewebe deutlich erhöhte und den Verlust des Alveolarknochens milderte.[6]
References:
[1] Cai C, et al. BCI Suppresses RANKL-Mediated Osteoclastogenesis and Alleviates Ovariectomy-Induced Bone Loss. Front Pharmacol. 2021 Nov 1;12:772540.
[2] Zhang B, et al. DUSP6 expression is associated with osteoporosis through the regulation of osteoclast differentiation via ERK2/Smad2 signaling. Cell Death Dis. 2021 Sep 2;12(9):825.
[3] Thompson EM, et al. The cytotoxic action of BCI is not dependent on its stated DUSP1 or DUSP6 targets in neuroblastoma cells. FEBS Open Bio. 2022 Jul;12(7):1388-1405.
[4] Duan S, et al. Loss of FBXO31-mediated degradation of DUSP6 dysregulates ERK and PI3K-AKT signaling and promotes prostate tumorigenesis. Cell Rep. 2021 Oct 19;37(3):109870.
[5] Feng X, et al. Aldosterone modulates thiazide-sensitive sodium chloride cotransporter abundance via DUSP6-mediated ERK1/2 signaling pathway. Am J Physiol Renal Physiol. 2015 May 15;308(10):F1119-27.
[6] Zhu C, et al. The therapeutic role of baicalein in combating experimental periodontitis with diabetes via Nrf2 antioxidant signaling pathway. J Periodontal Res. 2020 Jun;55(3):381-391.
| Cell experiment [1]: | |
Cell lines | MPNST cells |
Preparation Method | MPNST cells were starved overnight, incubated with BCI (2 uM) for 60 mins then stimulated with DMEM and 10% FBS for 1 hr. Immunoblot analysis of TP53, p-RB and p-ATM and PARP cleavage and CC3 in ST8814 and S462.TY MPNST cells 24h after treatment with BCI (2 uM). |
Reaction Conditions | 2 uM; 60 mins |
Applications | After 1 hr, p-ERK, p-JNK, p-c-jun and total c-jun were elevated in the BCI-treated MPNST cell lines ST8814 and S462.TY but did not change in iHSC-1λ. Within 24 hours, BCI decreased total PARP and increased cleaved PARP and CC3, indicative of apoptotic cell death in NF1 deficient ST8814 and S462.TY cells. |
| Animal experiment [2]: | |
Animal models | Female C57BL/6 mice (8-weeks old) |
Dosage form | 15 mg/kg or 30 mg/kg; i.p. |
Preparation method | Low- or high-concentration (15 mg/kg or 30 mg/kg) BCI was injected intraperitoneally for 8 weeks, and bone loss was evaluated by micro-CT. |
Applications | Bone loss was prevented in both the low- and high-concentration BCI groups. Moreover, quantitative results indicated obvious increases in bone volume/total tissue volume (BV/TV), trabecular number (Tb.N), bone mineral density (BMD), and bone surface density (BS/TV) in both BCI-treated groups relative to the OVX group. |
References: | |
| Cas No. | 1245792-51-1 | SDF | |
| Überlieferungen | (E)-BCI | ||
| Canonical SMILES | O=C1/C(C(NC2CCCCC2)C3=C1C=CC=C3)=C/C4=CC=CC=C4 | ||
| Formula | C22H23NO | M.Wt | 317.42 |
| Löslichkeit | DMSO: 125 mg/mL (393.80 mM) | Storage | Store at -20°C |
| General tips | Please select the appropriate solvent to prepare the stock solution according to the
solubility of the product in different solvents; once the solution is prepared, please store it in
separate packages to avoid product failure caused by repeated freezing and thawing.Storage method
and period of the stock solution: When stored at -80°C, please use it within 6 months; when stored
at -20°C, please use it within 1 month. To increase solubility, heat the tube to 37°C and then oscillate in an ultrasonic bath for some time. |
||
| Shipping Condition | Evaluation sample solution: shipped with blue ice. All other sizes available: with RT, or with Blue Ice upon request. | ||
| Prepare stock solution | |||
|
1 mg | 5 mg | 10 mg |
| 1 mM | 3.1504 mL | 15.752 mL | 31.504 mL |
| 5 mM | 0.6301 mL | 3.1504 mL | 6.3008 mL |
| 10 mM | 0.315 mL | 1.5752 mL | 3.1504 mL |
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Method for preparing in vivo formulation: Take μL DMSO master liquid, next add μL Corn oil, mix and clarify.
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- Purity: >98.00%
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Average Rating: 5 (Based on Reviews and 7 reference(s) in Google Scholar.)
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