Celecoxib (SC-58635)

카탈로그 번호S1261 배치:S126150

인쇄

기술 자료

화학식

C17H14F3N3O2S
분자량 381.37 CAS 번호 169590-42-5
용해도 (25°C)* 시험관 내(In vitro) DMSO 76 mg/mL (199.28 mM)
Ethanol 33 mg/mL (86.53 mM)
Water Insoluble
생체 내(In Vivo) (개별적으로 순서대로 용매를 제품에 첨가하십시오.)
Homogeneous suspension
CMC-NA
≥5mg/ml Taking the 1 mL working solution as an example, add 5 mg of this product to 1 ml of CMC-Na solution, mix evenly to obtain a homogeneous suspension with a final concentration of 5 mg/ml.
* <1 mg/ml은 약간 용해되거나 불용해됨을 의미합니다.
* Selleck은 모든 화합물의 용해도를 자체적으로 테스트하며, 실제 용해도는 게시된 값과 약간 다를 수 있습니다. 이는 정상적인 현상이며, 약간의 배치 간 변동으로 인해 발생합니다.
* 실온 배송 (안정성 테스트 결과 이 제품은 냉각 조치 없이 배송될 수 있음을 보여줍니다.)

원액 준비

생물학적 활성

설명 Celecoxib은 Sf9 세포에서 40 nM의 IC50을 갖는 선택적 COX-2 억제제입니다.
표적
COX-2
(Sf9 cells)
40 nM
시험관 내(In vitro)

Celecoxib은 15 μM의 IC50으로 COX-1에 대해 낮은 민감도를 보입니다. 이 화합물은 HNE1 및 CNE1-LMP1을 포함한 비인두암(NPC) 세포주에 대해 각각 32.86 μM 및 61.31 μM의 IC50으로 항증식 효과를 보입니다.

생체 내(In Vivo)

Celecoxib은 강력한 경구 항염증 활성을 나타냅니다. 이 화합물은 카라기난 부종 분석에서 급성 염증을, 보조제 유발 관절염 모델에서 만성 염증을 각각 ED50 7.1 mg/kg 및 0.37 mg/kg/day로 감소시킵니다. 또한, Hargreaves 과감각 모델에서 ED50 34.5 mg/kg으로 진통 활성도 나타냅니다. 이 외에도, 이 화학 물질은 200 mg/kg까지의 용량에서 쥐에게 급성 위장관 독성을 유발하지 않으며, 10일 동안 600 mg/kg/day까지의 용량에서 쥐에게 만성 위장관 독성을 유발하지 않습니다. C3Hf/KamLaw 암컷 쥐 모델에서, 단독으로 13.5 Gy 국소 흉부 방사선 조사(LTI) 후 중앙 생존 시간을 105일(범위, 79-145일)에서 142일(범위, 94-155일)로 증가시킵니다.

프로토콜 (참조)

키나아제 분석:

[1]
  • 체외 COX 효소 분석

    곤충 세포에서 COX 단백질의 발현은 COX-1 또는 COX-2 바큘로바이러스와 함께 3일 동안 배양된 세포의 균질액에서 PG 합성 능력을 평가하여 결정됩니다. COX-1 또는 COX-2를 발현하는 세포는 균질화되고 아라키돈산(10 μM)과 함께 배양됩니다. COX 활성은 PG 생산을 모니터링하여 결정됩니다. 모의 감염된 Sf9 세포에서는 COX 활성이 감지되지 않습니다. 이 화합물은 아라키돈산 첨가 전에 10분 동안 1% CHAPS 조 균질액(2-10 μg 단백질)과 함께 전배양됩니다. 형성된 PGE2는 10분 배양 후 ELISA에 의해 감지됩니다.
세포 분석:

[2]
  • 세포주

    HNE1 and CNE1-LMP1

  • 농도

    0-75 μM

  • 배양 시간

    48 hours

  • 방법

    The antiproliferative effect of Celecoxib on NPC cells is assessed using an MTT assay. Cells are seeded into 96-well plates and allowed to attach for 24 hours. The cells are then treated with increasing concentrations of this compound (0 to 75 μM) dissolved in DMSO (final concentration ≤0.1%) and incubated for up to 48 hours. After the incubation, 20 μL of MTT dye (5 mg/mL) are added to each well and cells are incubated at 37 °C for 4 hours. After removing the supernatants, the crystals are dissolved in DMSO and the absorbance is measured at 490 nm. The half-maximal inhibitory concentration (IC50) values and the 95% confidence intervals are calculated using probit regression using SPSS 15.0 software. The experiment is performed in triplicate and repeated at least three times.
동물 연구:

[1]
  • 동물 모델

    A 0.1 mL aliquot of a 1% solution of carrageenan in 0.9% sterile saline or 1 mg of Mycobacterium butyricum in 50 μL of mineral oil is administered to the right hind foot pad of male Sprague−Dawley rats.

  • 용량

    ≤200 mg/kg

  • 투여

    Administered via p.o.

참조

  • https://pubmed.ncbi.nlm.nih.gov/9135032/
  • https://pubmed.ncbi.nlm.nih.gov/22504904/
  • https://pubmed.ncbi.nlm.nih.gov/22672748/

고객 제품 검증

<p>Reduced hepatic lipid contents and alleviated liver injury in EC-AMPK mice treated with selective COX-2 inhibitors. Wild-type and EC-AMPK mice given a high fat diet were treated with vehicle, celecoxib or nimesulide for a period of 4 weeks. At the end of treatment, parameters including body weight and circulating glucose (A), serum triglyceride and cholesterol levels (B were measured and presented as percentage comparisons against those from vehicle-treated wild-type mice. *<em>P</em> < 0.05 versus wild-type mice treated with vehicle; #<em>P</em> < 0.05 versus EC-AMPK mice treated with vehicle, <em>n</em> = 3-5.</p>

데이터 출처 [ Br J Pharmacol , 2014 , 171(2), 498-508 ]

Breast cancer cells, wild type (WT) or anoikis resistant (AR) variants, were treated with celecoxib (CEL 5.0 uM) and/or sildenafil (SIL, 2.0 uM). Cells were isolated after 24h and viability determined by trypan blue exclusion (n = 3, +/- SEM) * p < 0.05 greater than corresponding value in vehicle control. Upper inset pictures: HCC38 cells in 96 well plates were treated with celecoxib (CEL 5.0 uM) and/or sildenafil (SIL, 2.0 uM). Cells were isolated after 24h and viability determined using a live-dead assay (red cells = dead; green cells = alive) (n = 3, +/- SEM) * p < 0.05 greater than corresponding value in vehicle control.

데이터 출처 [ J Cell Physiol , 2014 , 10.1002/jcp.24843 ]

Tumors were resected from mice 10 days after orthotopic inoculation of 4T1-Luc2 cells, and hydrogels loaded with the following payloads were evaluated: anti–PD-1, anti-CTLA-4, IL-15sa, lenalidomide, celecoxib, STING-RR, or R848. Mice that did not receive a hydrogel were examined as a negative control. (A) IVIS imaging of 4T1-Luc2 cells is shown for all groups described and illustrates tumor burden.

데이터 출처 [ , , Science, 2018, 10(433), doi: 10.1126/scitranslmed.aar1916 ]

Effect of celecoxib on the in vitro proliferation of BRAFV600E and NRASQ61R melanoma cell lines. a BRAFV600E A375 and NRASQ61R SK-MEL-2 melanoma cells were seeded at the density of 3 × 10<sup>3</sup> per well in a 96-well plate and incubated with the indicated concentrations of celecoxib. Untreated cells were used as a control. DMSO (vehicle of celecoxib) concentration was maintained at 0.02% in all wells. Following a 24 h incubation at 37℃ in a 5% CO2 atmosphere, growth inhibition was determined by MTT assay. Data are expressed as mean percent of proliferation ± SD of treated cells as compared to untreated control cells. Mean percent of proliferation and SD were calculated from three independent experiments performed in triplicate. Difference between doses of celecoxib was calculated using unpaired t-test. *** indicate P < 0.001. b BRAFV600E A375 and NRASQ61R SK-MEL-2 melanoma cells were seeded at the density of 4 × 10<sup>5</sup> per well in a 75 cm<sup>2</sup> tissue culture flask and incubated with celecoxib (60 μM). Untreated cells were used as a control. DMSO (vehicle of celecoxib) concentration was maintained at 0.02% in all wells. Following a 24 h incubation at 37℃ in a 5% CO2 atmosphere, viability of cells was determined by trypan blue assay. Data are expressed as mean percentage of viable (negative) and death cells (positive) of treated cells as compared to untreated control cells. *** indicate P < 0.001

데이터 출처 [ , , J Transl Med, 2017, 15(1):46 ]

Sellecks Celecoxib (SC-58635) 인용됨 115 출판물

Tumor-initiating stem cells fine-tune the plasticity of neutrophils to sculpt a protective niche [ Cancer Cell, 2025, S1535-6108(25)00494-5] PubMed: 41349542
Monkeypox virus induces ferroptosis to facilitate viral replication and promotes inflammatory responses [ Emerg Microbes Infect, 2025, 14(1):2522877] PubMed: 40536397
The nonsteroidal anti-inflammatory drug sulindac reverses obesity-driven immunosuppression and triple-negative breast cancer progression [ Breast Cancer Res, 2025, 27(1):186] PubMed: 41137072
Carbonic anhydrase 2-derived drug-responsive domain regulates membrane-bound cytokine expression and function in engineered T cells [ Commun Biol, 2025, 8(1):28] PubMed: 39789216
Hyperoxia-activated Nrf2 regulates ferroptosis in intestinal epithelial cells and intervenes in inflammatory reaction through COX-2/PGE2/EP2 pathway [ Mol Med, 2025, 31(1):1] PubMed: 39754066
Protein kinase a suppresses antiproliferative effect of interferon-α in hepatocellular carcinoma by activation of protein tyrosine phosphatase SHP2 [ J Biol Chem, 2025, 301(2):108195] PubMed: 39826687
Missense Mutant p53 Transactivates Wnt/β-Catenin Signaling in Neighboring p53-Destabilized Cells through the COX-2/PGE2 Pathway [ Cancer Res Commun, 2025, 5(1):13-23] PubMed: 39641656
Leptin-mediated suppression of lipoprotein lipase cleavage enhances lipid uptake and facilitates lymph node metastasis in gastric cancer [ Cancer Commun (Lond), 2024, 10.1002/cac2.12583] PubMed: 38958445
Therapeutic Anti-Tumor Efficacy of DC-Based Vaccines Targeting TME-Associated Antigens Is Improved When Combined with a Chemokine-Modulating Regimen and/or Anti-PD-L1 [ Vaccines (Basel), 2024, 12(7)777] PubMed: 39066414
Celecoxib Combined with Tocilizumab Has Anti-Inflammatory Effects and Promotes the Recovery of Damaged Cartilage via the Nrf2/HO-1 Pathway In Vitro [ Biomolecules, 2024, 14(12)1636] PubMed: 39766343

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