Ruxolitinib (INCB18424)

카탈로그 번호S1378 배치:S137821

인쇄

기술 자료

화학식

C17H18N6
분자량 306.37 CAS 번호 941678-49-5
용해도 (25°C)* 시험관 내(In vitro) DMSO 300 mg/mL (979.2 mM)
Ethanol 12 mg/mL (39.16 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.
Clear solution
5%DMSO 40%PEG 300 5%Tween80 50% ddH2O

Selleck 연구소에서 검증했습니다. 이 제형에 대한 조정이 필요한 경우 맞춤형 테스트를 위해 당사 영업팀에 문의하십시오.

 3.000mg/ml (9.79mM) Taking the 1 mL working solution as an example, add 50 μL of 60 mg/mL clarified DMSO stock solution to 400 μL PEG300, mix evenly to clarify it; add 50 μL Tween-80 to the above system, mix evenly to clarify it; then continue Add 500 μL ddH2O to adjust the volume to 1 mL. The mixed solution should be used immediately for optimal results. 
Clear solution
5%DMSO 95% Corn oil

Selleck 연구소에서 검증했습니다. 이 제형에 대한 조정이 필요한 경우 맞춤형 테스트를 위해 당사 영업팀에 문의하십시오.

 3.000mg/ml (9.79mM) Taking the 1 mL working solution as an example, add 50 μL of 60 mg/mL clear DMSO stock solution to 950 μL of corn oil and mix evenly. The mixed solution should be used immediately for optimal results. 
* <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 Ruxolitinib (INCB18424)은 무세포 분석에서 IC50 3.3 nM/2.8 nM을 나타내며 JAK3 대비 JAK1/2에 대해 130배 이상의 선택성을 가진, 임상에 진입한 최초의 강력하고 선택적인 JAK1/2 억제제입니다. 이 화합물은 toxic mitophagy를 통해 종양 세포를 사멸시킵니다. 또한 Autophagy를 유도하고 Apoptosis related 과정을 향상시킵니다.
표적
JAK2
(Cell-free assay)		 JAK1
(Cell-free assay)
2.8 nM 3.3 nM
시험관 내(In vitro) Ruxolitinib (INCB18424) potently and selectively inhibits JAK2V617F-mediated signaling and proliferation in Ba/F3 cells and HEL cells. This compound markedly increases apoptosis in a dose dependent manner in Ba/F3 cells. It (64 nM) results in a doubling of cells with depolarized mitochondria in Ba/F3 cells. This chemical inhibits proliferating of erythroid progenitors from normal donors and polycythemia vera patients with IC50 of 407 nM and 223 nM, respectively. It demonstrates remarkable potency against erythroid colony formation with IC50 of 67nM.
생체 내(In Vivo) INCB018424 (180 mg/kg, orally, twice a day) results in a survival rate of greater than 90% by day 22 in a JAK2V617F-driven mouse model. This compound (180 mg/kg, orally, twice a day) markedly reduces splenomegaly and circulating levels of inflammatory cytokines, and preferentially eliminates neoplastic cells, resulting in significantly prolonged survival without myelosuppressive or immunosuppressive effects in a JAK2V617F-driven mouse model. In the double-blind trial of myelofibrosis, the primary end point is reached in 41.9% of patients in the Ruxolitinib (INCB18424) group as compared with 0.7% in the placebo group. It results in maintaining reduction in spleen volume and improvement of 50% or more in the total symptom score. A total of 28% of the patients in the group receiving this compound (15 mg twice daily) has at least a 35% reduction in spleen volume at week 48 in patients with myelofibrosis, as compared with 0% in the group receiving the best available therapy. The mean palpable spleen length has decreased by 56% with it but has increased by 4% with the best available therapy at week 48. Patients in the ruxolitinib group has an improvement in overall quality-of-life measures and a reduction in symptoms associated with myelofibrosis.

프로토콜 (참조)

키나아제 분석:[1]
  • 결합 분석

    재조합 단백질은 Sf21 세포와 바큘로바이러스 벡터를 사용하여 발현되며 친화성 크로마토그래피로 정제됩니다. JAK 키나아제 분석은 펩타이드 기질(-EQEDEPEGDYFEWLE)을 이용한 균일 시간 분해 형광 분석법을 사용합니다. 각 효소 반응은 Ruxolitinib (INCB18424) 또는 대조군, JAK 효소, 500 nM 펩타이드, 아데노신 삼인산(ATP; 1mM) 및 2% 디메틸 설폭사이드(DMSO)를 사용하여 1시간 동안 수행됩니다. 50% 억제 농도(IC50)는 형광 신호의 50%를 억제하는 데 필요한 이 화합물의 농도로 계산됩니다.
세포 분석:[1]
  • 세포주

    Ba/F3 and HEL cells

  • 농도

    3 μM

  • 배양 시간

    48 hours

  • 방법

    Cells are seeded at 2 × 103/well of white bottom 96-well plates and treated with Ruxolitinib (INCB018424) from DMSO stocks (0.2% final DMSO concentration), followed by incubation for 48 hours at 37 ℃ with 5% CO2. Viability is measured by cellular ATP determination using the Cell-Titer Glo luciferase reagent or viable cell counting. Values are transformed to percent inhibition relative to vehicle control, and IC50 curves are fitted according to nonlinear regression analysis of the data using PRISM GraphPad.
동물 연구:[1]
  • 동물 모델

    JAK2V617F-driven mouse model

  • 용량

    180 mg/kg

  • 투여

    Oral gavage

참조

  • https://pubmed.ncbi.nlm.nih.gov/20130243/
  • https://pubmed.ncbi.nlm.nih.gov/22375971/
  • https://pubmed.ncbi.nlm.nih.gov/22375970/

고객 제품 검증

STAT3 phosphorylation as determined by phospho flow, mixed lymphocyte reactions containing BALB/c spleen-derived CD4+ T cells co-cultured with or without C57BL/6 BM-derived DC preactivated with 20 ng/mL LPS.

데이터 출처 [ Blood , 2014 , 123(24), 3832-42 ]

Miniscule 10 PFU amount of VA7-EGFP results in productive infection only in CT26LacZ cells whereas the self-limiting infection can be rescued with JAK/STAT inhibitor Ruxolitinib in CT26WT cells counteracting also the effects of exogenous IFNβ (100 U/ml) pre-treatment. Scale bar: 200 um.

데이터 출처 [ Gene Ther , 2014 , 10.1038/gt.2014.83 ]

BMDMs were isolated from wild-type mice and incubated in the different concentrations of Ruxolitinib for 1 h before stimulation with 500 U/ml IFN-β for 30 min. Levels of GAPDH as well as total and phospho-Tyr705 STAT3 were determined by immunoblotting.

데이터 출처 [ J Immunol , 2012 , 189(6), 2784-92 ]

<p> </p><p>HS578T cells were treated with indicated amount of inhibitor for 18 hr. The cells were lysed by cell lysis buffer (20 mM Tris-Cl (pH 8.0); 0.5 M NaCl; 0.25% Triton X-100; 1 mM EDTA; 1 mM EGTA; 10 mM β-glycerophosphate; 10 mM NaF; 300 µM Na3VO4; 1 mM benzamidine) containing 1 mM DTT and 2 µM PMSF. Western blot analyses were performed using cleared cell lysates resolved on sodium dodecyl sulfate (SDS)-polyacrylamide gels, transferred onto polyvinylidene difluoride (PVDF) membranes (Millipore, Billerica, MA), and probed with specific antibodies using standard procedures. Chemiluminescence reagent was purchased from  Thermo Scientific (Rockford, IL). Horseradish peroxidase-conjugated secondary antibodies from Sigma (St. Louis, MO).</p>

, , Yong Weon Yi Georgetown University

Selleck's Ruxolitinib (INCB18424) 인용됨 676 출판물

Systematic design of combination therapy by targeting master regulators of coexisting diffuse midline glioma cell states [ Nat Genet, 2026, 58(5):1112-1125.] PubMed: 42020604
Biomarkers of response to neoadjuvant palbociclib plus anastrozole in endocrine-resistant estrogen receptor-positive/HER2-negative breast cancer: a phase 2 trial [ Nat Commun, 2026, 17(1):949] PubMed: 41593097
Prolonged KRAS-MAPK Inhibition Induces Interferon Signaling that Promotes Cell State Transition and Confers Therapeutic Vulnerabilities [ Cancer Res, 2026, 10.1158/0008-5472.CAN-25-4114.] PubMed: 42008116
JAK1/2 inhibitor ruxolitinib reduces aggregates in cardiac proteinopathy [ EMBO Mol Med, 2026, 10.1038/s44321-026-00411-x] PubMed: 41917326
Wntless degradation mediated by CaMKII inhibition drives endoplasmic reticulum stress and apoptosis [ Cell Rep, 2026, 45(4):117256] PubMed: 41966825
ADA2-deficient cells exhibit increased levels of cell death and metabolic disturbances [ Cell Death Discov, 2026, 12(1)167] PubMed: 41866403
Non-gene-edited neural stem cells reverse neuroinflammation and microbiota dysbiosis in a sprague-dawley rat model of autism spectrum disorder [ Transl Psychiatry, 2026, 10.1038/s41398-026-03841-w] PubMed: 41922322
The tumor suppressor NDRG2 recruits protein phosphatase 2A to suppress STAT5 phosphorylation in adult T-cell leukemia/lymphoma [ J Biol Chem, 2026, S0021-9258(26)01952-6] PubMed: 42055322
Microbial metabolite drives ageing-related clonal haematopoiesis via ALPK1 [ Nature, 2025, 10.1038/s41586-025-08938-8] PubMed: 40269158
Macrophage-derived amphiregulin induces myofibroblast transition in adipogenic lineage precursors near Staphylococcus aureus abscess in bone marrow [ Nat Commun, 2025, 16(1):8409] PubMed: 40998791

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