Ruxolitinib (INCB018424)

For research use only.

Catalog No.S1378

284 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 284 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 NEPyNnRMcW6jc3WgRZN{[Xl? NHyzUpAzOCCvaX6= MVHEUXNQ MVvJcohq[mm2aX;uJI9nKEqDS{KgbY4hcHWvYX6gWGYyKGOnbHzzJIF{e2W|c3XkJIF{KGmwaHnibZRqd25ib3[gSXBQNWmwZIXj[YQhW1SDVEWgdIhwe3Cqb4L5cIF1cW:wIIfpeIghUUN3MDDv[kAxNjBzMt88US=> M17vWlIzPjl6MEi0
TF1 M2\0cmtqdmG|ZTDBd5NigQ>? M1PMT|IxKG2rbh?= M3nsPWROW09? NIfIWHRKdmirYnn0bY9vKG:oIFrBT|EhcW5iaIXtZY4hXEZzIHPlcIx{KGG|c3Xzd4VlKGG|IHnubIljcXSrb36gc4YhUUx4LXnu[JVk\WRiU2TBWFMheGixc4Doc5J6dGG2aX;uJJdqfGhiSVO1NEBw\iByLkCyOO69VQ>? Ml7xNlI3QThyOES=
Human T cell M{PvVmtqdmG|ZTDBd5NigQ>? Mo\HTY5pcWKrdHnvckBw\iCMQVuzM|EhcW5iaIXtZY4hXCClZXzsd{BmgHC{ZYPzbY5oKEOGMzDhd5Nme3OnZDDhd{BqdmirYnn0bY9vKG:oIFnMNk1{fGmvdXzheIVlKFOWQWS1ZUBxcG:|cHjvdplt[XSrb36ge4l1cCCLQ{WwJI9nKDBwMEKz{txO MUWyN|U1ODZ2OB?=
Human monocyte Ml63T4lv[XOnIFHzd4F6 MkftTY5pcWKrdHnvckBw\iCMQVuyJIlvKGi3bXHuJI1wdm:leYTld{BmgHC{ZYPzbY5oKEOGMUSgZZN{\XO|ZXSgZZMhcW6qaXLpeIlwdiCxZjDHUU1EW0Zvc4TpcZVt[XSnZDDTWGFVPWFicHjvd5Bpd3K7bHH0bY9vKHerdHigTWM2OCCxZjCwMlAzPs7:TR?= M{TlUVI{PTRyNkS4
Human monocyte NIjaZVRMcW6jc3WgRZN{[Xl? MX7Jcohq[mm2aX;uJI9nKEqDS{KvNUBqdiCqdX3hckBud26xY4n0[ZMh\XiycnXzd4lv\yCFREG0JIF{e2W|c3XkJIF{KGmwaHnibZRqd25ib3[gTWZP\2GvbXGtd5RqdXWuYYTl[EBUXEGWMTDwbI9{eGixconsZZRqd25id3n0bEBKSzVyIH;mJFAvODNzzszN M2XCN|I{PTRyNkS4
HEL MnL3R5l1d3SxeHnjJGF{e2G7 MkLPOUDPxE1? NXjxZYNsPDhiaB?= M{C1OmN6fG:2b4jpZ{BqdmSneE2xNk4zLQ>? NWH4T5ZIOjV7M{GzOFk>
SET-2 NEXXV3NEgXSxdH;4bYMhSXO|YYm= M4XIclUh|ryP NXG5Om5mPDhiaB?= Ml;jR5l1d3SxeHnjJIlv\GW6PUG4Mlcm NUe4U4JHOjV7M{GzOFk>
HT93A NGTLSGpIem:5dHigTY5pcWKrdHnvckBCe3OjeR?= MUizNlAhdk1? MV[1JIQ> NG\NdlJFVVOR Ml;yTY5pcWKrdHnvckBw\iCJQ2OtSkBqdmS3Y3XkJIdz[W63bH;jfZRq[yCmaX\m[ZJmdnSrYYTpc44> NV3XSZdZOjV6MEW5OlI>
CMK NUjqSZg3T3Kxd4ToJGlvcGmkaYTpc44hSXO|YYm= NXXXWphFUW6qaXLpeIlwdiCxZjDDUWsh[2G{conpcochfGinIFrBT|NCPTd{VjDteZRifGmxbjDj[YxtKHC{b3zp[oVz[XSrb36= NWjWVohoOjV|NUKxNlQ>
CMK MkjDS5Jwf3SqIFnubIljcXSrb36gRZN{[Xl? MV3Jcohq[mm2aX;uJI9nKEOPSzDjZZJzgWmwZzD0bIUhUkGNM1G2N2QhdXW2YYTpc44h[2WubDDwdo9tcW[ncnH0bY9vKHerdHigTWM2OCCxZjCwMlE3OyEQvF2= M2LnWVI2OzV{MUK0
CMK NIm1dI5Iem:5dHigTY5pcWKrdHnvckBCe3OjeR?= MV3Jcohq[mm2aX;uJI9nKEOPSzDjZZJzgWmwZzD0bIUhX1RiSlHLJINmdGxicILvcIln\XKjdHnvckB4cXSqIFnDOVAhd2ZiMD6wO|Uh|ryP M3PCUlI2OzV{MUK0
NCI-H460 NUm5UndFT3Kxd4ToJGlvcGmkaYTpc44hSXO|YYm= NEi0V5RFVVOR NGXDb|FKSzVyPUCuNVMh|ryP MnrSNlUzOTN4N{C=
NCI-H358 M1\wdGdzd3e2aDDJcohq[mm2aX;uJGF{e2G7 NH\MS2VFVVOR MW\JR|UxRTBwMTFOwG0> NHnXdmwzPTJzM{[3NC=>
A549 MXPHdo94fGhiSX7obYJqfGmxbjDBd5NigQ>? MljWSG1UVw>? NUDn[YJyUUN3ME2wMlA1KM7:TR?= NWT5U3JJOjV{MUO2O|A>
A549/DDP M3;kTGdzd3e2aDDJcohq[mm2aX;uJGF{e2G7 MUjEUXNQ NIf5XGFKSzVyPUCuNlIh|ryP NX3vWZAzOjV{MUO2O|A>
NCI-H1299 M2PtUGdzd3e2aDDJcohq[mm2aX;uJGF{e2G7 M3zhTmROW09? MWLJR|UxRTBwMkig{txO MkjZNlUzOTN4N{C=
NCI-H2347 MYHHdo94fGhiSX7obYJqfGmxbjDBd5NigQ>? M3HCRmROW09? NF;pNmtKSzVyPUCuNVch|ryP NXnBNo5mOjV{MUO2O|A>
A549/DDP M{\M[WZ2dmO2aX;uJGF{e2G7 Mn64N|Ahdk1? MWe0PEBp M37RPWROW09? MVnEc5dvNXKnZ4XsZZRqd25ib3[gV3RCXDNicHjvd5Bpd3K7bHH0bY9v MYeyOVIyOzZ5MB?=
NCI-H1299 M2jLPGZ2dmO2aX;uJGF{e2G7 M2LWWVMxKG6P NGHPW5Q1QCCq MW\EUXNQ NIj6SGlFd3ewLYLl[5Vt[XSrb36gc4YhW1SDVEOgdIhwe3Cqb4L5cIF1cW:w M{HrcVI2OjF|Nkew
NCI-H2347 NV;uTpp5TnWwY4Tpc44hSXO|YYm= NYPnN3AxOzBibl2= MWG0PEBp NWTvUZg2TE2VTx?= MUDE[YNz\WG|ZTDpckBD[2x{IHX4dJJme3Orb36= MUGyOVIyOzZ5MB?=
A549/DDP NGfheHlCeG:ydH;zbZMhSXO|YYm= MnnXN|Ahdk1? NXLDWpZKPDhiaB?= Mmn6SG1UVw>? NEfvRVFKdmS3Y4Tpc44hd2ZiYYDvdJRwe2m| MUWyOVIyOzZ5MB?=
NCI-H1299 NXnWfJROSXCxcITvd4l{KEG|c3H5 M{HIOlMxKG6P MkPYOFghcA>? NH;3SoFFVVOR MlnXTY5lfWO2aX;uJI9nKGGyb4D0c5Nqew>? MmHCNlUzOTN4N{C=
NCI-H2347 NHnicYRCeG:ydH;zbZMhSXO|YYm= NU\xfFAxOzBibl2= NILoS5U1QCCq M2G3TmROW09? NVzLTpZTUW6mdXP0bY9vKG:oIHHwc5B1d3Orcx?= MkjyNlUzOTN4N{C=
Hep3B NETzSVNHfW6ldHnvckBCe3OjeR?= M4rhXVEh|ryP MYexOkBp MU\EUXNQ NITyeZJKdXCjaYLld{B1cGViY3HwZYNqfHlib3[gTWhESS2jc4PvZ4lifGWmIHfwNVMxKG23dHHueJMhfG9iYXP0bZZmKFOWQWSzJJdqfGhiSVO1NEBw\iC-NUCg{txO MXeyOFUxOTZ6OR?=
HepG2 M2S1TWZ2dmO2aX;uJGF{e2G7 M2XZPFEh|ryP M4K4XVE3KGh? M2W0NGROW09? M3;PRmlueGGrcnXzJJRp\SClYYDhZ4l1gSCxZjDJTGNCNWG|c3;jbYF1\WRiZ4CxN|AhdXW2YX70d{B1dyC|aXfuZYwhfG9iU2TBWFM> MXuyOFUxOTZ6OR?=
Huh7 MUTGeY5kfGmxbjDBd5NigQ>? MojkNUDPxE1? MmP3NVYhcA>? NHzRe5hFVVOR M3[2XmlueGGrcnXzJJRp\SClYYDhZ4l1gSCxZjDJTGNCNWG|c3;jbYF1\WRiZ4CxN|AhdXW2YX70d{B1dyC|aXfuZYwhfG9iU2TBWFM> NVLx[mJzOjR3MEG2PFk>
BaF3 MVzLbY5ie2ViQYPzZZk> M3LIbFgxKG6P M{mwc|YhcA>? NWDxOXhXTE2VTx?= NHvRNY9T\WS3Y3XzJJRp\SCyaH;zdIhwenmuYYTpc44hd2cEoGPURXQ2KGmwIFrBT|JXPjF5Rj3teZRifGWmIFLBSlMuTVCRUjDj[Yxt NUjRNG9POjR{M{e3PVE>
DLD-1 MoHwT4lv[XOnIFHzd4F6 M1GyNVI2KM7:TR?= NWHzTI5HPDhiaB?= NWXQW4lFTE2VTx?= NIf1dGFKdmirYnn0bY9vKG:oIFrBT|EheGixc4Doc5J6dGG2aX;u MnnSNlQxPTB3NUC=
RKO MVLLbY5ie2ViQYPzZZk> Ml3ZNlUh|ryP M3f3U|Q5KGh? M1HVcGROW09? MorNTY5pcWKrdHnvckBw\iCMQVuxJJBpd3OyaH;yfYxifGmxbh?= MkTBNlQxPTB3NUC=
DLD-1 NUTLbHpRU2mwYYPlJGF{e2G7 M3vqT|I2KM7:TR?= M17iSFQ5KGh? NYLmNIxCTE2VTx?= NFrHSFRKdmirYnn0bY9vKG:oIFrBT|IheGixc4Doc5J6dGG2aX;u NV25[29COjRyNUC1OVA>
RKO NXLj[m1oU2mwYYPlJGF{e2G7 MkDBNlUh|ryP M2PTdFQ5KGh? M2[4fWROW09? M4TwdYRw\XNibn;0JIlvcGmkaYSgTmFMOSCyaH;zdIhwenmuYYTpc44> NEWzS3QzPDB3MEW1NC=>
DLD-1 NFLpd3RIem:5dHigTY5pcWKrdHnvckBCe3OjeR?= MX61NEDPxE1? MWq0PEBp NXHZbnRrTE2VTx?= M1nDVmlEPTB;MUWuOVEh|ryP Mon1NlQxPTB3NUC=
RKO M1vUfmdzd3e2aDDJcohq[mm2aX;uJGF{e2G7 M32zdlUxKM7:TR?= MYi0PEBp NIL4SIRFVVOR NUS3RW8{UUN3ME2xOE44PiEQvF2= M1;s[lI1ODVyNUWw
DLD-1 MmjIRZBweHSxc3nzJGF{e2G7 NYPMTG9{OjVizszN NHjCb2s1QCCq M2rtTWROW09? NFzHfoxKdmS3Y3XzJIFxd3C2b4Ppd{BjgSCjY4TpeoF1cW6pIHPhd5Bie2ViMx?= M4jNPFI1ODVyNUWw
RKO M4XSbGFxd3C2b4Ppd{BCe3OjeR?= MW[yOUDPxE1? MnPYOFghcA>? MVPEUXNQ M3XRe2lv\HWlZYOgZZBweHSxc3nzJIJ6KGGldHn2ZZRqdmdiY3HzdIF{\SB| Ml;GNlQxPTB3NUC=
HuH7 MoTvS5Jwf3SqIFnubIljcXSrb36gRZN{[Xl? M2LVSlUxKM7:TR?= M4LYZ|Q5KGh? NGDEV49FVVOR M4T3PV45OiVicnXkeYN1cW:w M4nJNlI{QTRzOEOy
SNU182 NWXlVohbT3Kxd4ToJGlvcGmkaYTpc44hSXO|YYm= NUfuR5JzPTBizszN NHzlXm01QCCq MYfEUXNQ MX6+OlQmKHKnZIXjeIlwdg>? NWnqXmtCOjN7NEG4N|I>
SNU423 NFXIZ4ZIem:5dHigTY5pcWKrdHnvckBCe3OjeR?= MUC1NEDPxE1? M{\sc|Q5KGh? MkTISG1UVw>? M3KxWV45OSVicnXkeYN1cW:w M3PUNFI{QTRzOEOy
HuH7 M4PSRWZ2dmO2aX;uJGF{e2G7 M4rzWFUxKM7:TR?= NWLqOHlUOjRiaB?= MoD4SG1UVw>? MmTkTY5pcWKrdHnvckBw\iCVVFHUNUBidmRiU2TBWFMheGixc4Doc5J6dGG2aX;uJJNq\26rZnnjZY51dHl? NFjJfnIzOzl2MUizNi=>
SNU182 MXLGeY5kfGmxbjDBd5NigQ>? NH;rV5M2OCEQvF2= NHL2U|EzPCCq MnXsSG1UVw>? MVzJcohq[mm2aX;uJI9nKFOWQWSxJIFv\CCVVFHUN{BxcG:|cHjvdplt[XSrb36gd4lodmmoaXPhcpRtgQ>? Mnz3NlM6PDF6M{K=
SNU423 MofJSpVv[3Srb36gRZN{[Xl? NHvkVGo2OCEQvF2= NXXFS49COjRiaB?= NWTpd5lKTE2VTx?= M3ruNmlvcGmkaYTpc44hd2ZiU2TBWFEh[W6mIGPURXQ{KHCqb4PwbI9zgWyjdHnvckB{cWewaX\pZ4FvfGy7 NIPwU40zOzl2MUizNi=>

... 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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Frequently Asked Questions

  • Question 1:

    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.

JAK Signaling Pathway Map

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Cell Lines Assay Type Concentration Incubation Time Formulation Activity Description PMID