Bottle, Media; Wheaton; Lab 45; Borosilicate glass; Autoclavable; With attached pour ring and 45mm pink screw cap; Wide mouth; Graduated; 500mL; Dia. x H: 86 x 186
Bottle, Media; Wheaton; Lab 45; Borosilicate glass; Autoclavable; With attached pour ring and 45mm pink screw cap; Wide mouth; Graduated; 500mL; Dia. x H: 86 x 186
Tyrosine kinase inhibitor is a potent tyrosine kinase inhibitor.
体外研究 (In Vitro)
Tyrosine kinases are important mediators of the signaling cascade, determining key roles in diverse biological processes like growth, differentiation, metabolism and apoptosis in response to external and internal stimuli[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
586.61
Formula
C31H31FN6O5
CAS 号
1021950-26-4
运输条件
Room temperature in continental US; may vary elsewhere.
[1]. Paul MK, et al. Tyrosine kinase – Role and significance in Cancer. Int J Med Sci. 2004;1(2):101-115.
[2]. Inoue T, et al. Two cases of gastrointestinal perforation after radiotherapy in patients receiving tyrosine kinase inhibitor for advanced renal cell carcinoma. World J Surg Oncol. 2012 Aug 20;10(1):167.
[3]. Bowen JM, et al. Development of a rat model of oral small molecule receptor tyrosine kinase inhibitor-induced diarrhea. Cancer Biol Ther. 2012 Nov 1;13(13).
[4]. Sun FK, et al. Multi-targeted tyrosine kinase inhibitor sunitinib: a novel strategy for sporadic malignant pheochromocytoma. Chin Med J (Engl). 2012 Jun;125(12):2231-4.
[5]. Thamm DH. Tyrosine kinase inhibitor special issue. Vet Comp Oncol. 2012 Sep;10(3):161-2. doi: 10.1111/j.1476-5829.2012.00339.x.
[6]. Eriksson A, et al. The novel tyrosine kinase inhibitor AKN-028 has significant antileukemic activity in cell lines and primary cultures of acute myeloid leukemia. Blood Cancer J. 2012 Aug 3;2:e81. doi: 10.1038/bcj.2012.28.
Emodin-d4 (Frangula emodin-d4) is the deuterium labeled Emodin. Emodin (Frangula emodin), an anthraquinone derivative, is an anti-SARS-CoV compound. Emodin blocks the SARS coronavirus spike protein and angiotensin-converting enzyme 2 (ACE2) interaction[1]. Emodin inhibits casein kinase-2 (CK2). Anti-inflammatory and anticancer effects[2]. Emodin is a potent selective 11β-HSD1 inhibitor with the IC50 of 186 and 86 nM for human and mouse 11β-HSD1, respectively. Emodin ameliorates metabolic disorder in diet-induced obese mice[3].
体外研究 (In Vitro)
Stable heavy isotopes of hydrogen, carbon, and other elements have been incorporated into drug molecules, largely as tracers for quantitation during the drug development process. Deuteration has gained attention because of its potential to affect the pharmacokinetic and metabolic profiles of drugs[1].
Shanghai Jinpan Biotech Co Ltd has not independently confirmed the accuracy of these methods. They are for reference only.
分子量
274.26
Formula
C15H6D4O5
CAS 号
132796-52-2
中文名称
大黄素 d4
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]. Russak EM, et al. Impact of Deuterium Substitution on the Pharmacokinetics of Pharmaceuticals. Ann Pharmacother. 2019;53(2):211-216.
[2]. Tin-Yun Ho, et al. Emodin blocks the SARS coronavirus spike protein and angiotensin-converting enzyme 2 interaction. Antiviral Res. 2007 May;74(2):92-101.
[3]. Stefania Sarno, et al. Toward the rational design of protein kinase casein kinase-2 inhibitors. Pharmacol Ther. Feb-Mar 2002;93(2-3):159-68.
[4]. Ying Feng, et al. Emodin, a natural product, selectively inhibits 11beta-hydroxysteroid dehydrogenase type 1 and ameliorates metabolic disorder in diet-induced obese mice. Br J Pharmacol. 2010 Sep;161(1):113-26.
Poloxin is a non-ATP competitive Polo-like Kinase 1 (PLK1) inhibitor that targets the polo-box domain, with an IC50 of appr 4.8 μM.
IC50 & Target[4]
PLK1 PBD
4.8 μM (IC50)
PLK2 PBD
18.7 μM (IC50)
PLK3 PBD
53.9 μM (IC50)
体外研究 (In Vitro)
Poloxin (25 μM) induces defects in centrosome integrity, spindle formation, and chromosome alignment in mitosis. Centrosomal fragmentation induced by Poloxin is partially rescued by Kiz T379E. Poloxin (25 μM) activates the mitotic checkpoint, induces apoptosis and inhibits proliferation of MDA-MB-231 cells[1]. Poloxin inhibits proliferation in both cell lines with a comparable efficiency through 72 h period[2]. Poloxin inhibits the polo-box domain (PBD) interaction with an apparent IC50 of ∼4.8 μM. Poloxin exhibits a loose Plk1 PBD specificity with 4-10 times higher IC50 values for Plk2 and Plk3, and does not significantly inhibit other types of phosphopeptide-binding domains such as FHA, WW, and SH2 domains[3].
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)
Poloxin (40 mg/kg) decreases the proliferation of MDA-MB-231 cells, and surpresses the growth of the tumor nude mice bearing established xenografts of MDA-MB-231[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
297.35
Formula
C18H19NO3
CAS 号
321688-88-4
运输条件
Room temperature in continental US; may vary elsewhere.
[1]. Yuan J, et al. Polo-box domain inhibitor poloxin activates the spindle assembly checkpoint and inhibits tumor growth in vivo. Am J Pathol. 2011 Oct;179(4):2091-9.
[2]. Sanhaji M, et al. p53 is not directly relevant to the response of Polo-like kinase 1 inhibitors. Cell Cycle. 2012 Feb 1;11(3):543-53.
[3]. Lee KS, et al. Pinning down the polo-box domain. Chem Biol. 2008 May;15(5):415-6.
[4]. Reindl W, et al. Inhibition of polo-like kinase 1 by blocking polo-box domain-dependent protein-protein interactions. Chem Biol. 2008 May;15(5):459-66.
Cell Assay [2]
Cell Viability Assay on treated cells in 96-well plates, based on viable cells. 20 μL of CellTiter-Blue®reagent is added to each well and then incubated at 37°C with 5% CO2 for 4h before fluorescence reading using a Victor 1420 Multilabel Counter. All experiments are performed in triplicate and at least three independent experiments are performed. Data are presented as percentage compared with control.
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 Administration [1]
Viable MDA-MB-231 or HeLa cells (1×106) are resuspended in 300 μL of 0.9% NaCl and s.c. injected into both flanks of nude mice (MDA-MB-231: n=8 mice in each group, total N=16; HeLa: n=7 mice in each group, total N=14). Approximately 3 weeks after inoculation, mice are treated with Poloxin (40 mg/kg) or TQ (20 mg/kg) by intratumoral injection on Mondays, Wednesdays, and Fridays for 5 to 6 weeks. The tumor area is calculated by multiplication of the greatest diameter with the perpendicular diameter every 2 to 3 days. Measurements of all tumors within the group are represented by the mean value. U-tests and Student’s t-tests are performed for statistical evaluation among MDA-MB-231 groups and between HeLa groups, respectively. All mice are properly treated in accordance with the guidelines of the local animal committee.
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]. Yuan J, et al. Polo-box domain inhibitor poloxin activates the spindle assembly checkpoint and inhibits tumor growth in vivo. Am J Pathol. 2011 Oct;179(4):2091-9.
[2]. Sanhaji M, et al. p53 is not directly relevant to the response of Polo-like kinase 1 inhibitors. Cell Cycle. 2012 Feb 1;11(3):543-53.
[3]. Lee KS, et al. Pinning down the polo-box domain. Chem Biol. 2008 May;15(5):415-6.
[4]. Reindl W, et al. Inhibition of polo-like kinase 1 by blocking polo-box domain-dependent protein-protein interactions. Chem Biol. 2008 May;15(5):459-66.
CCK2R Ligand-Linker Conjugates 1 Chemical Structure
CAS No. : 1452145-13-9
规格
是否有货
100 mg
询价
250 mg
询价
500 mg
询价
* Please select Quantity before adding items.
生物活性
CCK2R Ligand-Linker Conjugates 1 is a ligand-linker conjugate, which conjugates to the cytotoxic antimicrotubule agents Desacetyl Vinblastine Hydrazide (DAVBH) and Tubulysin B Hydrazide (TubBH) via a hydrophilic peptide linker[1].
分子量
1607.77
Formula
C72H110N12O27S
CAS 号
1452145-13-9
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]. Wayua C, et al. Selective Tumor Targeting of Desacetyl Vinblastine Hydrazide and Tubulysin B via Conjugation to a Cholecystokinin 2 Receptor (CCK2R) Ligand. Mol Pharm. 2015 Jul 6;12(7):2477-83.
Buparlisib Hydrochloride (BKM120 Hydrochloride) is a pan-class I PI3K inhibitor, with IC50 of 52 nM/166 nM/116 nM/262 nM for p110α/p110β/p110δ/p110γ, respectively.
IC50 & Target
p110α
52 nM (IC50)
p110β
166 nM (IC50)
p110δ
116 nM (IC50)
p110γ
262 nM (IC50)
Vps34
2.4 μM (IC50)
p110α-H1047R
58 nM (IC50)
p110α-E545K
99 nM (IC50)
mTOR
4.6 μM (IC50)
体外研究 (In Vitro)
Buparlisib (BKM120) exhibits 50-300 nM activity for class I PI3K’s, including the most common p110α mutants. Additionally, NVP-BKM120 exhibits lower potency against class III and class IV PI3K’s, where 2, 5, >5, and >25 μM biochemical activity is observed for inhibition of VPS34, mTOR, DNAPK, and PI4K, respectively[1]. Buparlisib (BKM120) induces multiple myeloma (MM) cell apoptosis in both dose- and time-dependent manners. Buparlisib (BKM120) at concentrations ≥10 μM induces significant apoptosis in all tested MM cell lines at 24 h (P<0.05, compares with control). Therefore, 10 μM Buparlisib (BKM120) and 24-h treatment are chose in in the following experiments if not stated otherwise. Buparlisib (BKM120) treatment results in a dose-dependent growth inhibition in all tested MM cell lines. Buparlisib (BKM120) IC50 varies among tested MM cells. At 24 h treatment, IC50 for ARP-1, ARK, and MM.1R is between 1 and 10 μM, while IC50 for MM.1S is <1 μm, and ic50 for U266 is between 10 and 100 μM. In summary, Buparlisib (BKM120) treatment results in MM cell growth inhibition and apoptosis in dose- and time-dependent manners[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)
In A2780 xenograft tumors, oral dosing of Buparlisib (BKM120) at 3, 10, 30, 60, and 100 mg/kg results in a dose dependent modulation of pAKTSer473. Partial inhibition of pAKTSer473 is observed at 3 and 10 mg/kg, and near complete inhibition is observed at doses of 30, 60, or 100 mg/kg, respectively. Inhibition of pAKT (normalized to total AKT) tracked well with both plasma and tumor drug exposure[1]. Mice receiving Buparlisib (BKM120) (5 μM per kg per day for 15 days) treatment has significantly smaller tumor burdens as compare with control mice, which are measured as tumor volume (P<0.05) and level of circulating human kappa chain (P<0.05). In addition, Buparlisib (BKM120) treatment significantly prolongs the survival of tumor-bearing mice (P<0.05)[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.
Clinical Trial
分子量
446.85
Formula
C18H22ClF3N6O2
CAS 号
1312445-63-8
中文名称
布帕尼西盐酸盐
运输条件
Room temperature in continental US; may vary elsewhere.
[1]. Burger MT, et al. Identification of NVP-BKM120 as a Potent, Selective, Orally Bioavailable Class I PI3 Kinase Inhibitor for Treating Cancer. ACS Med Chem Lett. 2011 Aug 26;2(10):774-9.
[2]. Zheng Y, et al. Novel phosphatidylinositol 3-kinase inhibitor NVP-BKM120 induces apoptosis in myeloma cells and shows synergistic anti-myeloma activity with dexamethasone. J Mol Med (Berl). 2012 Jun;90(6):695-706.
Cell Assay [1]
A2780 cells are cultured in DMEM supplemented with 10% FBS. L-glutamine, sodium pyruvate, and antibiotics. Cells are plated in the same medium at a density of 1000 cells per well, 100 uL per well into black-walled-clear-bottom plates and incubated for 3-5 hours. Buparlisib (BKM120) supplied in DMSO (20 mM) are diluted further into DMSO (7.5 uL of 20 mM NVP-BKM120 in 22.5 uL DMSO. Mix well, transfer 10 uL to 20 uL DMSO, repeat until 9 concentrations have been made). The diluted Buparlisib (BKM120) solution (2 uL), is then added to cell medium (500 uL) cell medium. Equal volumes of this solution (100 uL) are added to the cells in 96 well plates and incubated at 37ºC for 3 days and developed using Cell Titer Glo. Inhibition of cell proliferation is determined by luminescence read using Trilux[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 Administration [2]
Mice[2] Six- to eight-week-old female severe combined immunodeficiency (SCID) mice are used. SCID mice are subcutaneously inoculated in the right flank with 1 million ARP-1 or MM.1S cells suspended in 50 μL phosphate-buffered saline (PBS). After palpable tumor developed (tumor diameter ≥5 mm), mice are treated with intraperitoneal injection of DMSO/PBS or Buparlisib (BKM120) (5 μM per kg per day) for 15 days. Tumor sizes are measured every 5 days, and blood samples are collected at the same period. Tumor burdens are evaluated by measuring tumor size and detecting circulating human kappa chain or lambda chain.
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]. Burger MT, et al. Identification of NVP-BKM120 as a Potent, Selective, Orally Bioavailable Class I PI3 Kinase Inhibitor for Treating Cancer. ACS Med Chem Lett. 2011 Aug 26;2(10):774-9.
[2]. Zheng Y, et al. Novel phosphatidylinositol 3-kinase inhibitor NVP-BKM120 induces apoptosis in myeloma cells and shows synergistic anti-myeloma activity with dexamethasone. J Mol Med (Berl). 2012 Jun;90(6):695-706.
Alendronic acid-d6 is the deuterium labeled Alendronic acid. Alendronic acid, a bisphosphonate, is a farnesyl diphosphate synthase (FDPS) inhibitor. Alendronic acid inhibits osteoclast-mediated bone resorption. Alendronic acid shows efficacy in postmenopausal osteoporosis, malignant hypercalcemia and Paget’s disease[1].
体外研究 (In Vitro)
Stable heavy isotopes of hydrogen, carbon, and other elements have been incorporated into drug molecules, largely as tracers for quantitation during the drug development process. Deuteration has gained attention because of its potential to affect the pharmacokinetic and metabolic profiles of drugs[1].
Shanghai Jinpan Biotech Co Ltd has not independently confirmed the accuracy of these methods. They are for reference only.
分子量
255.13
Formula
C4H7D6NO7P2
CAS 号
1035437-39-8
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]. Russak EM, et al. Impact of Deuterium Substitution on the Pharmacokinetics of Pharmaceuticals. Ann Pharmacother. 2019;53(2):211-216.
[2]. Teixeira S, et al. Alendronic Acid as Ionic Liquid: New Perspective on Osteosarcoma. Pharmaceutics. 2020 Mar 24;12(3). pii: E293.
[3]. Duckworth AD, et al. Effect of Alendronic Acid on Fracture Healing: A Multicenter Randomized Placebo-Controlled Trial. J Bone Miner Res. 2019 Jun;34(6):1025-1032.
Nanocs fluorescent labeled gold nanoparticles were made from monodispersed gold nanoparticles with narrow size distribution (<15%). Fluorescent molecules, from green to near infrared region, including fluorescein (FITC), rhodamine, Cy3, Cy5 or Alexa fluor dyes, were convalently attached to the gold surface. These fluorescently labeled gold nanoparticles are stable in aqueous buffer and is useful for generating various gold nanoparticle probes to detect various biomolecules in SEM, TEM, light microscopy and blotting.
Physical Properties:
Organe, red, purple or blue depends on composition;
(R)-(-)-Ibuprofen is the R enantiomer of Ibuprofen, inactive on COX, inhibits NF-κB activation; (R)-(-)-Ibuprofen exhibits anti-inflammatory and antinociceptive effects.
IC50 & Target
NF-κB
体外研究 (In Vitro)
(R)-(-)-Ibuprofen is the R enantiomer of Ibuprofen, with no inhibitory effect on COX, but is involved in pathways of lipid metabolism and is incorporated into triglycerides along with endogenous fatty acids[1]. (R)-(-)-Ibuprofen (1 μM) significantly reduces NF-κB activation and completely prevents NF-κB induction at 10 μM. (R)-(-)-Ibuprofen inhibits NF-κB luciferase activity with an IC50 of 121.8 μM, weaker than that of S(+)-ibuprofen (IC50, 61.7 μM). Furthermore, (R)-(-)-Ibuprofen (10 mM) has no effect on HSF[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.
分子量
206.28
Formula
C13H18O2
CAS 号
51146-57-7
中文名称
(R)-(-)-布洛芬
运输条件
Room temperature in continental US; may vary elsewhere.
[1]. Evans AM, et al. Comparative pharmacology of S(+)-ibuprofen and (RS)-ibuprofen. Clin Rheumatol. 2001 Nov;20 Suppl 1:S9-14.
[2]. Scheuren N, et al. Modulation of transcription factor NF-kappaB by enantiomers of the nonsteroidal drug ibuprofen. Br J Pharmacol. 1998 Feb;123(4):645-52.
Neratinib-d6 (HKI-272-d6) is the deuterium labeled Neratinib. Neratinib (HKI-272) is an orally available, irreversible tyrosine kinase inhibitor with IC50s of 59 nM and 92 nM for HER2 and EGFR, respectively.
体外研究 (In Vitro)
Stable heavy isotopes of hydrogen, carbon, and other elements have been incorporated into drug molecules, largely as tracers for quantitation during the drug development process. Deuteration has gained attention because of its potential to affect the pharmacokinetic and metabolic profiles of drugs[1].
Shanghai Jinpan Biotech Co Ltd has not independently confirmed the accuracy of these methods. They are for reference only.
分子量
563.08
Formula
C30H23D6ClN6O3
CAS 号
1259519-18-0
中文名称
来那替尼 d6
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]. Russak EM, et al. Impact of Deuterium Substitution on the Pharmacokinetics of Pharmaceuticals. Ann Pharmacother. 2019;53(2):211-216.
[2]. Rabindran SK, et al. Antitumor activity of HKI-272, an orally active, irreversible inhibitor of the HER-2 tyrosine kinase. Cancer Res, 2004, 64(11), 3958-3965.
[3]. Yoshioka T, et al. Antitumor activity of pan-HER inhibitors in HER2-positive gastric cancer. Cancer Sci. 2018 Apr;109(4):1166-1176.
PI4KIII beta inhibitor 3 is a novel and high effective PI4KIIIβ inhibitor with IC50 of 5.7 nM.
IC50 & Target[1]
PI4KIIIβ
5.7 nM (IC50)
体外研究 (In Vitro)
PI4KIII beta inhibitor 3 is a PI4KIII inhibitor extracted from patent WO/2013034738 A1, the compound of formula 3, has an IC50 of 5.7 nM. PI4KIII beta inhibitor 3 exerts significant immunosuppressive activity, with IC50 value of 3 nM in the mixed lymphocyte reaction (MLR) assay. PI4KIII beta inhibitor 3 inhibits IL2 and IFNy secretion with IC50 values of less than InM in each case. Thus, PI4KIII beta inhibitor 3 is shown to be as effective at inhibiting IL2 and IFNy secretion as conventional immunosuppressants such as cyclosporine A. IC50 on IFNy and IL-2 release of Cyclosporine A are 2nM and less than 1 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)
PI4KIII beta inhibitor 3 (40 mg/kg per day, n=12) is able to delay the onset of arthritic symptoms and also to decrease symptom severity in a preventive model of arthritis compared to a vehicle control (MC 1%, n=12). PI4KIII beta inhibitor 3 reduces the anti-CII IgG titre and histological scores in the collagen-induced arthritis mouse model. Oral administration of PI4KIII beta inhibitor 3 results in prolonged graft survival in 3 out of 6 grafts in each group at day 30. Several grafts continued beating after withdrawal of the treatment (up to 60 days), indicating the induction of a certain type of graft tolerance. To evaluate the operational tolerance phenotype, animals with functional graft at day 60 are challenged with a second graft from the same donor strain or from a third party. No treatment is applied. The second grafts from the third party are rejected at day 8 (n=2) whereas second grafts from the same donor strain are functional for more than 90 days (n=2)[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
446.53
Formula
C22H22N8OS
CAS 号
1245319-54-3
运输条件
Room temperature in continental US; may vary elsewhere.
[1]. Jean Herman, et al. Autoimmune and inflammatory disorder therapy. From PCT Int. Appl. (2013), WO 2013034738 A1
Animal Administration [1]
Mice[1] DBA1 male mice, 8-10 weeks old, are distributed in 2 groups according to the treatment. Twelve animals received daily treatment with vehicle (1% methylcellulose), twelve others receive PI4KIII beta inhibitor 3 at 40 mg/kg/d in 1% methylcellulose. The treatment initiation started the day before the intradermal injection at the base of the tail of 100 μg of emulsified chicken collagen II in presence of complete Freund adjuvant and added heat-killed Mycobacterium butyricum. Daily inspection of the mice is performed to weight animals and quantify disease score according to the following scale (score 0: normal; score 1 : redness and/or swelling in one joint; score 2: redness and/or swelling in more than one joint; score 3: redness and/or swelling in the entire paw; score 4: deformity and/or ankylosis). On the day of sacrifice (day 42) serum are collected and anti-collagen II antibody titers are determined by ELISA. Joints are harvested, fixed in 6% paraformaldehyde, decalcified in formic acid 6% for 48 h, sliced and stained by hematoxylin and eosin staining. Hyperplasia of the synovium, infiltration of mono and polymorphonuclear cells and pannus formation parameters are scored blindly.
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]. Jean Herman, et al. Autoimmune and inflammatory disorder therapy. From PCT Int. Appl. (2013), WO 2013034738 A1
Colcemid-d3 (Demecolcine-d3) is the deuterium labeled Colcemid. Colcemid (Demecolcine), a derivative of colchicine, is a potent mitotic inhibitor[1][2]. Colcemid binds to the protein tubulin and arrest cells in metaphase for karyotyping assays. Colcemid incuces cell apoptosis and can be used for cancer research[2].
体外研究 (In Vitro)
Stable heavy isotopes of hydrogen, carbon, and other elements have been incorporated into drug molecules, largely as tracers for quantitation during the drug development process. Deuteration has gained attention because of its potential to affect the pharmacokinetic and metabolic profiles of drugs[1].
Shanghai Jinpan Biotech Co Ltd has not independently confirmed the accuracy of these methods. They are for reference only.
分子量
374.45
Formula
C21H22D3NO5
CAS 号
1217668-72-8
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]. Russak EM, et al. Impact of Deuterium Substitution on the Pharmacokinetics of Pharmaceuticals. Ann Pharmacother. 2019;53(2):211-216.
[2]. T Tsuchida, et al. Colcemid-induced apoptosis of cultured human glioma: electron microscopic and confocal laser microscopic observation of cells sorted in different phases of cell cycle. Cytometry. 1998 Apr 1;31(4):295-9.
[3]. Ashley M Rozario, et al. Ultra-Low Colcemid Doses Induce Microtubule Dysfunction as Revealed by Super-Resolution Microscopy. Bioexiv.
UNC1215 is a potent and selective inhibitor for the methyllysine (Kme) reading domain function of L3MBTL3 with a Kd value of 120 nM and an IC50 of 40 nM. UNC1215 has the potential to treat malignant brain tumor.
IC50 & Target
IC50: 40 nM (L3MBTL3). Kd: 120 nM (L3MBTL3).
体外研究 (In Vitro)
UNC1215 binds L3MBTL3 with a d of 120 nM, competitively displacing mono- or dimethyllysine-containing peptides, and is greater than 50-fold more potent toward L3MBTL3 than other members of the MBT family while also demonstrating selectivity against more than 200 other reader domains examined. X-ray crystallography identified a unique 2:2 polyvalent mode of interaction between UNC1215 and L3MBTL3. In cells, UNC1215 is nontoxic and directly binds L3MBTL3 via the Kme-binding pocket of the MBT domains. UNC1215 increases the cellular mobility of GFP-L3MBTL3 fusion proteins, and point mutants that disrupt the Kme-binding function of GFP-L3MBTL3 phenocopy the effects of UNC1215 on localization[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
529.72
Formula
C32H43N5O2
CAS 号
1415800-43-9
运输条件
Room temperature in continental US; may vary elsewhere.
[1]. James LI, Barsyte-Lovejoy D, Zhong N, et al. Discovery of a chemical probe for the L3MBTL3 methyllysine reader domain. Nat Chem Biol. 2013 Mar;9(3):184-91. doi: 10.1038/nchembio.1157.