FT709 is a potent and selective USP9X inhibitor, an IC50 of 82 nM. USP9X has been linked with centrosome function, chromosome alignment during mitosis, EGF receptor degradation, chemo-sensitization, and circadian rhythms[1].
分子量
498.51
Formula
C23H22N4O7S
CAS 号
2413991-74-7
运输条件
Room temperature in continental US; may vary elsewhere.
储存方式
Please store the product under the recommended conditions in the Certificate of Analysis.
参考文献
[1]. Clancy A, et, al. The deubiquitylase USP9X controls ribosomal stalling. J Cell Biol. 2021 Mar 1;220(3):e202004211.
FT3967385 is a novel USP30 inhibitor that recapitulates genetic loss of USP30 and sets the trigger for PINK1-PARKIN amplification of mitochondrial ubiquitylation.
分子量
373.41
Formula
C21H19N5O2
运输条件
Room temperature in continental US; may vary elsewhere.
储存方式
Please store the product under the recommended conditions in the Certificate of Analysis.
参考文献
[1]. Rusilowicz-Jones E, et al. A novel USP30 inhibitor recapitulates genetic loss of USP30 and sets the trigger for PINK1-PARKIN amplification of mitochondrial ubiquitylation. BioRxiv. 2020 April 20.
FT3967385 is a novel USP30 inhibitor that recapitulates genetic loss of USP30 and sets the trigger for PINK1-PARKIN amplification of mitochondrial ubiquitylation.
分子量
373.41
Formula
C21H19N5O2
运输条件
Room temperature in continental US; may vary elsewhere.
储存方式
Please store the product under the recommended conditions in the Certificate of Analysis.
参考文献
[1]. Rusilowicz-Jones E, et al. A novel USP30 inhibitor recapitulates genetic loss of USP30 and sets the trigger for PINK1-PARKIN amplification of mitochondrial ubiquitylation. BioRxiv. 2020 April 20.
FT3967385 is a novel USP30 inhibitor that recapitulates genetic loss of USP30 and sets the trigger for PINK1-PARKIN amplification of mitochondrial ubiquitylation.
分子量
373.41
Formula
C21H19N5O2
运输条件
Room temperature in continental US; may vary elsewhere.
储存方式
Please store the product under the recommended conditions in the Certificate of Analysis.
参考文献
[1]. Rusilowicz-Jones E, et al. A novel USP30 inhibitor recapitulates genetic loss of USP30 and sets the trigger for PINK1-PARKIN amplification of mitochondrial ubiquitylation. BioRxiv. 2020 April 20.
FT-1518 is a new generation selective, potent and oral bioavailable mTORC1 and mTORC2 inhibitor, and exhibits antitumor activity.
IC50 & Target[1]
mTORC1
mTORC2
体外研究 (In Vitro)
FT-1518 is a new generation selective, potent and oral bioavailable mTORC1 and mTORC2 inhibitor, and exhibits antitumor activity. FT-1518 displays significant growth inhibitory activity against a large panel of hematologic and solid tumor cell lines with most activities falling into low nanomolar range. FT-1518 cuases potent inhibition of the mTOR pathway biomarkers (mTORC 1 & 2 biomarkers [pAkt(S473) and pS6(S240/244) or p70 S6K), no inhibition of PI3K biomarker [pAkt(T308)] in cells[1].
上海金畔生物科技有限公司 has not independently confirmed the accuracy of these methods. They are for reference only.
体内研究 (In Vivo)
FT-1518 exhibits dose-dependent and higher tumor growth inhibition (TGI) in multiple solid tumor xenografts[1].
上海金畔生物科技有限公司 has not independently confirmed the accuracy of these methods. They are for reference only.
分子量
394.47
Formula
C20H26N8O
CAS 号
1313026-58-2
运输条件
Room temperature in continental US; may vary elsewhere.
储存方式
Please store the product under the recommended conditions in the Certificate of Analysis.
参考文献
[1]. Alain C. Mita, et al. Abstract 137: FT-1518, a new generation selective and potent mTORC1 and mTORC2 inhibitor: an in vitro and in vivo profile. Cancer Res 2017;77(13 Suppl).
FT113 is a potent and orally active fatty acid synthase (FASN) inhibitor, with an IC50 of 213 nM for full-length recombinant human FASN enzyme. In cell-based assay, FT113 blocks FASN activity in BT474 cells (IC50, 90 nM). FT113 shows anti-proliferative activity, and exhibits anti-cancer activity both in vitro and in vivo[1].
IC50 & Target
IC50: 213 nM (FASN), 90 nM (FASN, in BT474 cell)[1]
体外研究 (In Vitro)
FT113 shows anti-proliferative activity against PC3 and MV-411 cells with IC50s of 47 and 26 nM, respectively[1].
上海金畔生物科技有限公司 has not independently confirmed the accuracy of these methods. They are for reference only.
体内研究 (In Vivo)
FT113 (5 mg/kg, p.o.) exhibits potent oral bioavailability of 95% and 84% in mice and rats, respectively[1]. FT113 (5, 25, or 50 mg/kg, p.o., twice daily for 16 days) increases malonyl-CoA concentration in tumors, inhibits tumor growth in a dose-dependent manner in mice[1].
上海金畔生物科技有限公司 has not independently confirmed the accuracy of these methods. They are for reference only.
Animal Model:
Athymic nude mice bearing MV-411 cells[1]
Dosage:
5, 25, or 50 mg/kg
Administration:
P.O., twice daily for 16 days
Result:
Caused 32 % and 50% tumor growth inhibition at 25 and 50 mg/kg, respectively in mice.
分子量
409.41
Formula
C22H20FN3O4
CAS 号
1630808-89-7
运输条件
Room temperature in continental US; may vary elsewhere.
[1]. Martin MW, et al. Discovery and optimization of novel piperazines as potent inhibitors of fatty acid synthase (FASN). Bioorg Med Chem Lett. 2019 Apr 15;29(8):1001-1006.
Tegafur(Synonyms: 替加氟; FT 207; NSC 148958) 纯度: 99.96%
Tegafur (FT 207; NSC 148958) 是抗癌剂5-FU的前药。
Tegafur Chemical Structure
CAS No. : 17902-23-7
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10 mM * 1 mL in DMSO
￥726
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100 mg
￥660
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￥1200
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生物活性
Tegafur (FT 207; NSC 148958) is a chemotherapeutic 5-FU prodrug used in the treatment of cancers; is a component of tegafur-uracil.
IC50 & Target
Nucleoside antimetabolite/analog
体外研究 (In Vitro)
Tegafur is bioactivated to 5-FU by liver microsomal cytochrome P450 enzymes. 5-FU is subsequently converted into its active metabolites 5-fluoro-deoxyuridine-monophosphate (FdUMP) and 5-fluorouridine-triphosphate (FUTP) intracellularly; these metabolites inhibit the enzyme thymidylate synthase and intercalate into RNA, resulting in decreased thymidine synthesis, reduced DNA synthesis, disrupted RNA function, and tumor cell cytotoxicity.
上海金畔生物科技有限公司 has not independently confirmed the accuracy of these methods. They are for reference only.
Clinical Trial
分子量
200.17
Formula
C8H9FN2O3
CAS 号
17902-23-7
中文名称
替加氟；呋喃氟尿嘧啶；呋氟尿嘧啶
运输条件
Room temperature in continental US; may vary elsewhere.
[1]. Sotaro Sadahiro, Toshiyuki Suzuki, Akira Tanaka, et al. Association of right-sided tumors with high thymidine phosphorylase gene expression levels and the response to oral uracil and tegafur/leucovorin chemotherapy among patients with colorectal cancer. Cancer Chemotherapy and Pharmacology. 2012, 70 (2): 285-291.
[2]. José L. Ariasa, et al. Engineering of an antitumor (core/shell) magnetic nanoformulation based on the chemotherapy agent ftorafur. Colloids and Surfaces A: Physicochemical and Engineering Aspects. 2011,384(1-3): 157-163.
[3]. Gabriel N. Hortobagyi, William Heim, Laura Hutchins, et al. A phase 2 study of a fixed combination of uracil and ftorafur (UFT) and leucovorin given orally in a 3-times-daily regimen to treat patients with recurrent metastatic breast cancer. Cancer. 2010, 116(6): 1440-1445.
[4]. K. Fujita, H. Nakayama, W. Ichikawa, et al. Pharmacokinetics of 5-Fluorouracil in Elderly Japanese Patients with Cancer Treated with S-1 (a Combination of Tegafur and Dihydropyrimidine Dehydrogenase Inhibitor 5-Chloro-2,4-dihydroxypyridine). Drug Metab Dispos. 2009 Jul;37(7):1375-7. doi: 10.1124/dmd.109.027052. Epub 2009 Apr 23.
FT671 is a potent, non-covalent and selective USP7 inhibitor with an IC50 of 52 nM and binds to the USP7 catalytic domain with a Kd of 65 nM.
IC50 & Target
IC50: 52 nM (USP7)[1]
Kd: 65 nM (USP7)[1]
体外研究 (In Vitro)
FT671 increases p53 protein levels in HCT116 or bone osteosarcoma (U2OS) cell lines, leading to induction of p53 target genes including BBC3 (which encodes PUMA), CDKN1A (p21), RPS27L (S27L) and MDM2. FT671 leads to the degradation of N-Myc and upregulation of p53 in the neuroblastoma cell line IMR-32. FT671 also stabilizes p53 in the MM.1S multiple myeloma cell line, which correlates with increased MDM2 ubiquitination and leads to expression of p53 target genes[1].
上海金畔生物科技有限公司 has not independently confirmed the accuracy of these methods. They are for reference only.
体内研究 (In Vivo)
FT671 (100 mg/kg and 200 mg/kg, Oral gavage, daily) treatment in mice leads to a significant dose-dependent inhibition of tumor growth. And FT671 is well-torelated even at high doses[1].
上海金畔生物科技有限公司 has not independently confirmed the accuracy of these methods. They are for reference only.
Animal Model:
Non-obese diabetic-severe combined immunodeficient (NOD–SCID) mice implanted with MM.1S cells[1].
Dosage:
100 mg/kg and 200 mg/kg.
Administration:
Oral gavage daily.
Result:
Led to a significant dose-dependent inhibition of tumor growth.
分子量
533.48
Formula
C24H23F4N7O3
CAS 号
1959551-26-8
运输条件
Room temperature in continental US; may vary elsewhere.
FT827 is a selective and covalent ubiquitin-specific protease 7 (USP7) inhibitor (Ki=4.2 µM). FT827 binds to the USP7 catalytic domain (USP7CD; residues 208-560) with an apparent Kd value of 7.8 µM[1].
IC50 & Target
Ki: 4.2 μM (USP7); Kd: 7.8 μM (USP7)[1]
体外研究 (In Vitro)
FT827 features a vinylsulfonamide moiety that covalently modifies the catalytic Cys223 of USP7 and inhibits the enzyme with Ki and Kd of 4.2 and 7.8 μM, respectively. FT827 exclusively inhibit USP7 in a panel of 38 deubiquitinases (DUBs) from diverse families. FT827 inhibits USP7 probe reactivity with IC50s of 0.1-2 µM, confirming 10 to 100-fold higher potency as compared to P22077 in crude cell extracts or with intact MCF7 breast cancer cells, followed by incubation with the ubiquitin active site suicide probe haemagglutinin (HA)-tagged ubiquitin bromoethyl (HA-UbC2Br)[1].
上海金畔生物科技有限公司 has not independently confirmed the accuracy of these methods. They are for reference only.
分子量
548.61
Formula
C27H28N6O5S
CAS 号
1959537-86-0
运输条件
Room temperature in continental US; may vary elsewhere.
[1]. Turnbull AP, et al. Molecular basis of USP7 inhibition by selective small-molecule inhibitors. Nature. 2017 Oct 26;550(7677):481-486.
Kinase Assay [1]
To determine compound IC50s, FT827 is diluted in 100% DMSO in three-fold 12- point dilution series from 100 µM. 100 nL of 100-fold concentrated solutions are dispensed into black 384-well plate. 25 nM ubiquitin-rhodamine 110, along with recombinant USP7CD (3 nM), or USP7C-term (30-125 pM, depending on batch activity) are added and the plates incubated at room temperature for 1 h. The reaction is terminated by adding 2.5 µL citric acid to a final concentration of 10 mM prior to measuring fluorescence intensity on a Pherastar with a 485 nm excitation/520 nm emission optic module[1].
上海金畔生物科技有限公司 has not independently confirmed the accuracy of these methods. They are for reference only.
参考文献
[1]. Turnbull AP, et al. Molecular basis of USP7 inhibition by selective small-molecule inhibitors. Nature. 2017 Oct 26;550(7677):481-486.
Olutasidenib (FT-2102) is a highly potent, orally active, brain penetrant and selective inhibitor of mutant Isocitrate dehydrogenase 1 (IDH1), with IC50 values of 21.2 nM and 114 nM for IDH1- R132H and IDH1- R132C, respectively . Olutasidenib (FT-2102) is under the study in the treatment of acute myeloid leukemia (AML) or myelodysplastic syndrome (MDS) [1][2].
Olutasidenib (FT-2102) potently inhibits 2-HG production by multiple IDH1-R132 mutants (R132H, R132C, R132G, R132L), suggesting Olutasidenib (FT-2102) could be efficacious against most IDH1-R132 mutant-expressing tumors. Olutasidenib (FT-2102) is highly selective for IDH1 isoforms, showing no appreciable inhibition against wild-type IDH1 (> 20 µM) and IDH2 mutants (R172K and R140Q: both > 20 µM)[2].
上海金畔生物科技有限公司 has not independently confirmed the accuracy of these methods. They are for reference only.
体内研究 (In Vivo)
Olutasidenib (FT-2102, three oral doses (12.5, 25, and 50 mg/kg) in 12-hour intervals) exhibits potent anti-tumor activity in HCT116-IDH1-R132H/+ xenograft bearing female BALB/c Nude mice[2].
上海金畔生物科技有限公司 has not independently confirmed the accuracy of these methods. They are for reference only.
Three oral doses (12.5, 25, and 50 mg/kg) in 12-hour intervals.
Result:
Showed a time and dose-dependent inhibition of 2-HG levels in in tumor. At the highest dose tested in these studies (50 mg/kg), treatment with FT-2102 inhibited 2-HG levels in the tumor by >90% for up to 24 hours after the last dose in the HCT116-IDH1-R132H/+ xenograft model.
Clinical Trial
分子量
354.79
Formula
C18H15ClN4O2
CAS 号
1887014-12-1
运输条件
Room temperature in continental US; may vary elsewhere.
[1]. JM Watts, et al. A phase 1 dose escalation study of the IDH1m inhibitor, FT-2102, in patients with acute myeloid leukemia (AML) or myelodysplastic syndrome (MDS).
[2]. Justin A. Caravella, et al. Structure-based design and identification of FT-2102 (olutasidenib), a potent mutant-selective IDH1 inhibitor. J Med Chem. 2020.
