Ruxolitinib (INCB018424)

For research use only.

Catalog No.S1378

277 publications

Ruxolitinib (INCB018424) Chemical Structure

Molecular Weight(MW): 306.37

Ruxolitinib (INCB018424) is the first potent, selective, JAK1/2 inhibitor to enter the clinic with IC50 of 3.3 nM/2.8 nM in cell-free assays, >130-fold selectivity for JAK1/2 versus JAK3. Ruxolitinib kills tumor cells through toxic mitophagy. Ruxolitinib induces autophagy and enhances apoptosis.

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Selleck's Ruxolitinib (INCB018424) has been cited by 277 publications

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Choose Selective JAK Inhibitors

Biological Activity

Description Ruxolitinib (INCB018424) is the first potent, selective, JAK1/2 inhibitor to enter the clinic with IC50 of 3.3 nM/2.8 nM in cell-free assays, >130-fold selectivity for JAK1/2 versus JAK3. Ruxolitinib kills tumor cells through toxic mitophagy. Ruxolitinib induces autophagy and enhances apoptosis.
Targets
JAK2 [1]
(Cell-free assay)
JAK1 [1]
(Cell-free assay)
2.8 nM 3.3 nM
In vitro

INCB018424 potently and selectively inhibits JAK2V617F-mediated signaling and proliferation in Ba/F3 cells and HEL cells. INCB018424 markedly increases apoptosis in a dose dependent manner in Ba/F3 cells. INCB018424 (64 nM) results in a doubling of cells with depolarized mitochondria in Ba/F3 cells. INCB018424 inhibits proliferating of erythroid progenitors from normal donors and polycythemia vera patients with IC50 of 407 nM and 223 nM, respectively. INCB018424 demonstrates remarkable potency against erythroid colony formation with IC50 of 67nM. [1]

Cell Data
Cell Lines Assay Type Concentration Incubation Time Formulation Activity Description PMID
TF1 NGLrdG5McW6jc3WgRZN{[Xl? MYiyNEBucW5? NIXxRnhFVVOR MlW0TY5pcWKrdHnvckBw\iCMQVuyJIlvKGi3bXHuJHRHOSClZXzsd{Bie3Onc4Pl[EBieyCrbnjpZol1cW:wIH;mJGVRVy2rbnT1Z4VlKFOWQWS1JJBpd3OyaH;yfYxifGmxbjD3bZRpKEmFNUCgc4YhOC5yMUNOwG0> MlrRNlI3QThyOES=
TF1 NVv4bItRU2mwYYPlJGF{e2G7 MUGyNEBucW5? MoKzSG1UVw>? NYLtV2dUUW6qaXLpeIlwdiCxZjDKRWsyKGmwIHj1cYFvKFSIMTDj[YxteyCjc4Pld5Nm\CCjczDpcohq[mm2aX;uJI9nKEmONj3pcoR2[2WmIGPURXQ{KHCqb4PwbI9zgWyjdHnvckB4cXSqIFnDOVAhd2ZiMD6wNlTPxE1? MkTRNlI3QThyOES=
Human T cell M3ftU2tqdmG|ZTDBd5NigQ>? NGm4XGVKdmirYnn0bY9vKG:oIFrBT|MwOSCrbjDoeY1idiCWIHPlcIx{KGW6cILld5NqdmdiQ1SzJIF{e2W|c3XkJIF{KGmwaHnibZRqd25ib3[gTWwzNXO2aX31cIF1\WRiU2TBWFViKHCqb4PwbI9zgWyjdHnvckB4cXSqIFnDOVAhd2ZiMD6wNlPPxE1? NXjkbI11OjN3NEC2OFg>
Human monocyte M1vpWmtqdmG|ZTDBd5NigQ>? M1m3fGlvcGmkaYTpc44hd2ZiSlHLNkBqdiCqdX3hckBud26xY4n0[ZMh\XiycnXzd4lv\yCFREG0JIF{e2W|c3XkJIF{KGmwaHnibZRqd25ib3[gS20uS1OILYP0bY12dGG2ZXSgV3RCXDWjIIDoc5NxcG:{eXzheIlwdiC5aYToJGlEPTBib3[gNE4xOjcQvF2= MYKyN|U1ODZ2OB?=
Human monocyte MmjIT4lv[XOnIFHzd4F6 NEPme|BKdmirYnn0bY9vKG:oIFrBT|IwOSCrbjDoeY1idiCvb37vZ5l1\XNiZYjwdoV{e2mwZzDDSFE1KGG|c3Xzd4VlKGG|IHnubIljcXSrb36gc4YhUU[QZ3HtcYEue3SrbYXsZZRm\CCVVFHUNUBxcG:|cHjvdplt[XSrb36ge4l1cCCLQ{WwJI9nKDBwMEOx{txO MUmyN|U1ODZ2OB?=
HEL NVzNbHNpS3m2b4TvfIlkKEG|c3H5 NHH4WIU2KM7:TR?= NImyS401QCCq NW\3NHVoS3m2b4TvfIlkKGmwZHX4QVEzNjJn NGO4[WozPTl|MUO0PS=>
SET-2 NIHETIdEgXSxdH;4bYMhSXO|YYm= Mke3OUDPxE1? MV20PEBp NX[3e5NTS3m2b4TvfIlkKGmwZHX4QVE5Njdn NGXiNFczPTl|MUO0PS=>
HT93A NH;y[29Iem:5dHigTY5pcWKrdHnvckBCe3OjeR?= Mlq0N|IxKG6P MVy1JIQ> MV;EUXNQ MYXJcohq[mm2aX;uJI9nKEeFUz3GJIlv\HWlZXSg[5JidnWub3P5eIlkKGSrZn\ldoVvfGmjdHnvci=> MmP2NlU5ODV7NkK=
CMK MXPHdo94fGhiSX7obYJqfGmxbjDBd5NigQ>? NFzNSZJKdmirYnn0bY9vKG:oIFPNT{Bk[XK{eXnu[{B1cGViSlHLN2E2PzKYIH31eIF1cW:wIHPlcIwheHKxbHnm[ZJifGmxbh?= Ml7SNlU{PTJzMkS=
CMK NHTLZ|RIem:5dHigTY5pcWKrdHnvckBCe3OjeR?= NF3Td25KdmirYnn0bY9vKG:oIFPNT{Bk[XK{eXnu[{B1cGViSlHLN2E3O0RibYX0ZZRqd25iY3XscEBxem:uaX\ldoF1cW:wIIfpeIghUUN3MDDv[kAxNjF4MzFOwG0> MoXlNlU{PTJzMkS=
CMK MXTHdo94fGhiSX7obYJqfGmxbjDBd5NigQ>? NX3xb2p3UW6qaXLpeIlwdiCxZjDDUWsh[2G{conpcochfGinIGfUJGpCUyClZXzsJJBzd2yrZnXyZZRqd25id3n0bEBKSzVyIH;mJFAvODd3IN88US=> NVK1WVMzOjV|NUKxNlQ>
NCI-H460 M17Ddmdzd3e2aDDJcohq[mm2aX;uJGF{e2G7 NGD6eIxFVVOR M4TabGlEPTB;MD6xN{DPxE1? MX:yOVIyOzZ5MB?=
NCI-H358 MnLSS5Jwf3SqIFnubIljcXSrb36gRZN{[Xl? NVjvRYo3TE2VTx?= NETBUXBKSzVyPUCuNUDPxE1? NITpenczPTJzM{[3NC=>
A549 MmDaS5Jwf3SqIFnubIljcXSrb36gRZN{[Xl? MVLEUXNQ NXKweJZLUUN3ME2wMlA1KM7:TR?= MUSyOVIyOzZ5MB?=
A549/DDP NUDDZ5pCT3Kxd4ToJGlvcGmkaYTpc44hSXO|YYm= MVTEUXNQ MULJR|UxRTBwMkKg{txO NXTCe4x2OjV{MUO2O|A>
NCI-H1299 M3vjZWdzd3e2aDDJcohq[mm2aX;uJGF{e2G7 NWPZU3V3TE2VTx?= MWPJR|UxRTBwMkig{txO NWflVm9DOjV{MUO2O|A>
NCI-H2347 NEjUNnhIem:5dHigTY5pcWKrdHnvckBCe3OjeR?= NHzINYtFVVOR M4P4dmlEPTB;MD6xO{DPxE1? MYWyOVIyOzZ5MB?=
A549/DDP MkG2SpVv[3Srb36gRZN{[Xl? MVezNEBvVQ>? MYm0PEBp NXrKWFVQTE2VTx?= NFLocWVFd3ewLYLl[5Vt[XSrb36gc4YhW1SDVEOgdIhwe3Cqb4L5cIF1cW:w MUGyOVIyOzZ5MB?=
NCI-H1299 M1H6ZmZ2dmO2aX;uJGF{e2G7 MWWzNEBvVQ>? NFjhNlY1QCCq NWHNT|k3TE2VTx?= NIT0bXNFd3ewLYLl[5Vt[XSrb36gc4YhW1SDVEOgdIhwe3Cqb4L5cIF1cW:w MWCyOVIyOzZ5MB?=
NCI-H2347 NFLCZ|NHfW6ldHnvckBCe3OjeR?= MkXSN|Ahdk1? M1X6ZVQ5KGh? M2fpN2ROW09? NUnWNJJtTGWlcnXhd4UhcW5iQnPsNkBmgHC{ZYPzbY9v MXuyOVIyOzZ5MB?=
A549/DDP M1nEXGFxd3C2b4Ppd{BCe3OjeR?= Mm\uN|Ahdk1? M2fze|Q5KGh? MVHEUXNQ MoezTY5lfWO2aX;uJI9nKGGyb4D0c5Nqew>? MorkNlUzOTN4N{C=
NCI-H1299 MYDBdI9xfG:|aYOgRZN{[Xl? NU\xZpc6OzBibl2= Ml6wOFghcA>? NEDjTYtFVVOR M3PC[2lv\HWldHnvckBw\iCjcH;weI9{cXN? NIXsbGIzPTJzM{[3NC=>
NCI-H2347 MnK5RZBweHSxc3nzJGF{e2G7 NHzjO4U{OCCwTR?= NHf5b4E1QCCq MmjvSG1UVw>? NHzre|NKdmS3Y4Tpc44hd2ZiYYDvdJRwe2m| M3myR|I2OjF|Nkew
Hep3B M3izd2Z2dmO2aX;uJGF{e2G7 NFrIc|IyKM7:TR?= NVHYfYVLOTZiaB?= MYnEUXNQ MoWxTY1x[Wm{ZYOgeIhmKGOjcHHjbZR6KG:oIFnIR2Eu[XO|b3PpZZRm\CCpcEGzNEBufXSjboTzJJRwKGGldHn2[UBUXEGWMzD3bZRpKEmFNUCgc4YhhjVyIN88US=> NVvx[ZBJOjR3MEG2PFk>
HepG2 NEW2OFJHfW6ldHnvckBCe3OjeR?= NUfkVpk2OSEQvF2= MUexOkBp NUnWXVJXTE2VTx?= MmG3TY1x[Wm{ZYOgeIhmKGOjcHHjbZR6KG:oIFnIR2Eu[XO|b3PpZZRm\CCpcEGzNEBufXSjboTzJJRwKHOrZ37hcEB1dyCVVFHUNy=> NXfJdpg{OjR3MEG2PFk>
Huh7 NGT6SFNHfW6ldHnvckBCe3OjeR?= MlmwNUDPxE1? NW[0eJR7OTZiaB?= MULEUXNQ Mnu0TY1x[Wm{ZYOgeIhmKGOjcHHjbZR6KG:oIFnIR2Eu[XO|b3PpZZRm\CCpcEGzNEBufXSjboTzJJRwKHOrZ37hcEB1dyCVVFHUNy=> MUeyOFUxOTZ6OR?=
BaF3 M4rFN2tqdmG|ZTDBd5NigQ>? NX;peWEzQDBibl2= NHnI[Yk3KGh? MlnuSG1UVw>? MlPOVoVlfWOnczD0bIUheGixc4Doc5J6dGG2aX;uJI9nyqCVVFHUOUBqdiCMQVuyWlYyP0ZvbYX0ZZRm\CCEQV[zMWVRV1JiY3XscC=> NXq1coQzOjR{M{e3PVE>
DLD-1 MVHLbY5ie2ViQYPzZZk> M{j4S|I2KM7:TR?= NGXiRYY1QCCq MmDXSG1UVw>? MW\Jcohq[mm2aX;uJI9nKEqDS{GgdIhwe3Cqb4L5cIF1cW:w NYf6TpVjOjRyNUC1OVA>
RKO MWrLbY5ie2ViQYPzZZk> MXeyOUDPxE1? MYm0PEBp M{TXT2ROW09? MlvjTY5pcWKrdHnvckBw\iCMQVuxJJBpd3OyaH;yfYxifGmxbh?= MofENlQxPTB3NUC=
DLD-1 NFfydW5McW6jc3WgRZN{[Xl? NH[5cmszPSEQvF2= NIP1dpE1QCCq MUjEUXNQ MofrTY5pcWKrdHnvckBw\iCMQVuyJJBpd3OyaH;yfYxifGmxbh?= NV\pR|UxOjRyNUC1OVA>
RKO MYTLbY5ie2ViQYPzZZk> M{DOUFI2KM7:TR?= MXS0PEBp M1PsdWROW09? NHTtNoJld2W|IH7veEBqdmirYnn0JGpCUzFicHjvd5Bpd3K7bHH0bY9v M2LITVI1ODVyNUWw
DLD-1 MlrxS5Jwf3SqIFnubIljcXSrb36gRZN{[Xl? NYDlV3dLPTBizszN NYHaSGU5PDhiaB?= MULEUXNQ MVLJR|UxRTF3LkWxJO69VQ>? M2TXR|I1ODVyNUWw
RKO NVHYRZZoT3Kxd4ToJGlvcGmkaYTpc44hSXO|YYm= MV[1NEDPxE1? M1jw[FQ5KGh? NHT5RYZFVVOR MXrJR|UxRTF2Lke2JO69VQ>? MWGyOFA2ODV3MB?=
DLD-1 NI\KWndCeG:ydH;zbZMhSXO|YYm= MXGyOUDPxE1? NELIPFQ1QCCq M4HoV2ROW09? NYXVOHc6UW6mdXPld{BieG:ydH;zbZMh[nliYXP0bZZifGmwZzDjZZNx[XOnIEO= NVm0RnFHOjRyNUC1OVA>
RKO MYTBdI9xfG:|aYOgRZN{[Xl? NETTUoYzPSEQvF2= NHP3V|c1QCCq MXnEUXNQ MU\JcoR2[2W|IHHwc5B1d3OrczDifUBi[3SrdnH0bY5oKGOjc4Dhd4UhOw>? M{LofFI1ODVyNUWw
HuH7 NXHkSHN3T3Kxd4ToJGlvcGmkaYTpc44hSXO|YYm= NYT5RlNIPTBizszN MYO0PEBp NUDvXI5FTE2VTx?= M3H5NV45OiVicnXkeYN1cW:w M2TTXFI{QTRzOEOy
SNU182 MV3Hdo94fGhiSX7obYJqfGmxbjDBd5NigQ>? MV61NEDPxE1? NXTvZ2Q6PDhiaB?= NE\XWI9FVVOR M{DR[F43PCVicnXkeYN1cW:w M1PhVFI{QTRzOEOy
SNU423 NHXIcIFIem:5dHigTY5pcWKrdHnvckBCe3OjeR?= NGTh[Jc2OCEQvF2= MWK0PEBp MVTEUXNQ M1HZVl45OSVicnXkeYN1cW:w Mnq2NlM6PDF6M{K=
HuH7 MXnGeY5kfGmxbjDBd5NigQ>? MnjIOVAh|ryP MnLsNlQhcA>? NIfTVGdFVVOR M17C[2lvcGmkaYTpc44hd2ZiU2TBWFEh[W6mIGPURXQ{KHCqb4PwbI9zgWyjdHnvckB{cWewaX\pZ4FvfGy7 MWKyN|k1OTh|Mh?=
SNU182 NUfuUWdYTnWwY4Tpc44hSXO|YYm= NEDVPVQ2OCEQvF2= NIXxVpIzPCCq NWD2OYwyTE2VTx?= NIGyWnFKdmirYnn0bY9vKG:oIGPURXQyKGGwZDDTWGFVOyCyaH;zdIhwenmuYYTpc44he2mpbnnmbYNidnSueR?= NETYe3IzOzl2MUizNi=>
SNU423 M3;Te2Z2dmO2aX;uJGF{e2G7 NXvHZVMxPTBizszN NVj6dIFNOjRiaB?= MWHEUXNQ M1XoUmlvcGmkaYTpc44hd2ZiU2TBWFEh[W6mIGPURXQ{KHCqb4PwbI9zgWyjdHnvckB{cWewaX\pZ4FvfGy7 NHnKRWYzOzl2MUizNi=>

... Click to View More Cell Line Experimental Data

Assay
Methods Test Index PMID
Western blot
cleaved PARP / cleaved caspase3; 

PubMed: 29849942     


OVCAR-8 and MDAH 2774 cells were incubated with various concentrations of ruxolitinib for 48 h. Apoptosis was determined by using cleaved poly-ADP ribose polymerase (PARP) and cleaved caspase-3 by Western blot.

p-JAK2 / p-AKT / p-MAPK / Bcl-xl / MCL-1; 

PubMed: 29849942     


OVCAR-8 and MDAH2774 cells were treated with ruxolitinib (20 μM), paclitaxel (10 nM) or the combination for 24 h. Whole cells were collected and determined for the change of STAT3, AKT and ERK pathways and expression of BCL-XL and MCL-1 by Western blot.

c-Myc / c-Jun / Cyclin B / Cyclin D / Bcl-2 / HIF-1α; 

PubMed: 30930994     


Effects of ruxolitinib on the expression of downstream target genes of the JAK-STAT pathway. The protein levels of c-Myc, c-Jun, Cyclin B1, Cyclin D1, Bcl-2 and HIF-1α were determined in MCF-7 and TAMR-MCF-7 cells 24 h following ruxolitinib treatment (0.1-10 μM). 

p-STAT3; 

PubMed: 29849942     


Dose-dependent inhibition of STAT3 phosphorylation. Human ovarian cancer cells, OVCAR-8, MDAH2774, and SKOV3, were treated with the indicated concentrations of ruxolitinib for 24 h. Phosphorylation of STAT3 was analyzed by Western blot. 

29849942 30930994
Growth inhibition assay
Cell viability; 

PubMed: 29849942     


Dose dependent inhibition of cell viability. Human ovarian cancer cell lines were treated with the indicated concentrations of ruxolitinib. Cell viability was determined 72 h later. The IC50 was determined by the Chou-Talalay method. *P<0.05; ***P<0.0005, ruxolitinib vs control in OVCAR-8 cells; #P<0.05; ##P<0.005; ###P<0.0005, ruxolitinib vs control in SKOV-3 cells; ^^P<0.005; ^^^P<0.0005, ruxolitinib vs control in MDAH2774 cells.

Cell apoptosis; 

PubMed: 29849942     


OVCAR-8 and MDAH 2774 cells were incubated with various concentrations of ruxolitinib for 48 h. Apoptosis was determined by flow cytometry using annexin V and PI staining.

Cell proliferation; 

PubMed: 29515770     


Cells were plated into 48 well plates and cell growth was measured every 48 hours via MTS assay following ruxolitinib treatment (0, 1, 10 and 100 uM) in L-428 (left) and HDLM-2 (middle) HL cells, and Karpas-1106P PMBL cells (right).

29849942 29515770
Immunofluorescence
α-tubulin; 

PubMed: 26356819     


Confocal analysis of HEL cells, treated or not with different concentration of ruxolitinib (100 and 300 nM), displaying α-Tubulin (green) and DAPI (blue) staining; MERGE shows the overlapped images. Scale bars are shown in the figure (10 μm). Note more diffuse microtubule networks in ruxolutinib-treated cells.

26356819
In vivo INCB018424 (180 mg/kg, orally, twice a day) results in survive rate of greater than 90% by day 22 in a JAK2V617F-driven mouse model. INCB018424 (180 mg/kg, orally, twice a day) markedly reduces splenomegaly and circulating levels of inflammatory cytokines, and preferentially eliminated neoplastic cells, resulting in significantly prolonged survival without myelosuppressive or immunosuppressive effects in a JAK2V617F-driven mouse model. [1] The primary end point is reached in 41.9% of patients in the Ruxolitinib group as compared with 0.7% in the placebo group in the double-blind trial of myelofibrosis. Ruxolitinib results in maintaining of reduction in spleen volume and improvement of 50% or more in the total symptom score. [2] A total of 28% of the patients in the Ruxolitinib (15 mg twice daily) group 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 Ruxolitinib 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. [3]

Protocol

Kinase Assay:[1]
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Binding assay:

Recombinant proteins are expressed using Sf21 cells and baculovirus vectors and purified with affinity chromatography. JAK kinase assays use a homogeneous time-resolved fluorescence assay with the peptide substrate (-EQEDEPEGDYFEWLE). Each enzyme reaction is carried out with Ruxolitinib or control, JAK enzyme, 500 nM peptide, adenosine triphosphate (ATP; 1mM), and 2% dimethyl sulfoxide (DMSO) for 1 hour. The 50% inhibitory concentration (IC50) is calculated as INCB018424 concentration required for inhibition of 50% of the fluorescent signal.
Cell Research:[1]
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  • Cell lines: Ba/F3 and HEL cells
  • Concentrations: 3 μM
  • Incubation Time: 48 hours
  • Method: Cells are seeded at 2 × 103/well of white bottom 96-well plates, treated with INCB018424 from DMSO stocks (0.2% final DMSO concentration), and incubated 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.
    (Only for Reference)
Animal Research:[1]
- Collapse
  • Animal Models: JAK2V617F-driven mouse model
  • Dosages: 180 mg/kg
  • Administration: Oral gavage
    (Only for Reference)

Solubility (25°C)

In vitro DMSO 61 mg/mL (199.1 mM)
Ethanol 61 mg/mL (199.1 mM)
Water Insoluble
In vivo Add solvents to the product individually and in order(Data is from Selleck tests instead of citations):
2% DMSO+30% PEG 300+ddH2O
For best results, use promptly after mixing.
5mg/mL

* Please note that Selleck tests the solubility of all compounds in-house, and the actual solubility may differ slightly from published values. This is normal and is due to slight batch-to-batch variations.

Chemical Information

Molecular Weight 306.37
Formula

C17H18N6

CAS No. 941678-49-5
Storage powder
in solvent
Synonyms N/A
Smiles N#CCC(C1CCCC1)[N]2C=C(C=N2)C3=NC=NC4=C3C=C[NH]4

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Clinical Trial Information

NCT Number Recruitment interventions Conditions Sponsor/Collaborators Start Date Phases
NCT04359290 Not yet recruiting Drug: Ruxolitinib administration ARDS Human|COVID Philipps University Marburg Medical Center May 2020 Phase 2
NCT03774082 Recruiting Drug: INC424 Graft vs Host Disease Novartis Pharmaceuticals|Novartis May 29 2020 Phase 2
NCT04361903 Not yet recruiting Drug: Ruxolitinib Oral Tablet Severe Acute Respiratory Syndrome Coronavirus 2 Azienda USL Toscana Nord Ovest|Fondazione C.N.R./Regione Toscana G. Monasterio Pisa Italy|Azienda Ospedaliera Universitaria Senese|Azienda Ospedaliero Universitaria Pisana April 25 2020 --
NCT04057573 Recruiting Drug: Ruxolitinib cream|Drug: Vehicle Non-segmental Vitiligo Incyte Corporation October 3 2019 Phase 3

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    What is the difference between S2902 and S1378 which seem to have same structure formula according to the product information?

  • Answer:

    These two chemicals are the two different chiral forms of Ruxolitinib. S2902 S-Ruxolitinib is the S form and S1378 Ruxolitinib is the D form. One of the carbon atoms in this molecule is asymmetric, making the two molecules mirror images of each other. The biological activities of these two molecules can be very different because of the confirmation differences.

  • Question 2:

    How about the half-life of the compound (Ruxolitinib)? How long is the duration of the inhibitory effect on JAK-STAT signaling?

  • Answer:

    The half-life of this compound in body is about 2~3 hours according to previous study. Generally, it is longer in vitro culture medium than in vivo. In paper, Ruxolitinib was also used for 24hours. http://www.bloodjournal.org/cgi/pmidlookup?view=long&pmid=24711661.

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Cell Lines Assay Type Concentration Incubation Time Formulation Activity Description PMID