Doramapimod (BIRB 796)

Catalog No.S1574

Doramapimod (BIRB 796) Chemical Structure

Molecular Weight(MW): 527.66

Doramapimod (BIRB 796) is a pan-p38 MAPK inhibitor with IC50 of 38 nM, 65 nM, 200 nM and 520 nM for p38α/β/γ/δ in cell-free assays, and binds p38α with Kd of 0.1 nM in THP-1 cells, 330-fold greater selectivity versus JNK2, weak inhibition for c-RAF, Fyn and Lck, insignificant inhibition of ERK-1, SYK, IKK2.

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In DMSO USD 294 In stock
USD 147 In stock
USD 270 In stock
USD 470 In stock
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Cited by 18 Publications

5 Customer Reviews

  • Lympho-myeloid potential assessed by FACS analysis of human CD19 (B-lymphoid cells) and CD33/CD15 (myeloid cells) in bone marrow of NSG recipient mice, 17 weeks after transplantation. Each plot represents an animal from the experiment presented in panel.

    Blood 2012 119(26), 6255-8. Doramapimod (BIRB 796) purchased from Selleck.

    Effect of blockade of p38 or MEK on MK2 activation following TLR stimulation in moDC. MoDC were pre-treated with p38 inhibitors SB203580 10 mM (S), BIRB0796 (B) 0.1 or 1.0 mM or MEK inhibitor UO126 10 mM (U) for 1hr followed by poly I:C/R848 stimulation for 30 min then Western blotted for p-MK2 with β-actin loading control.

    Int J Cancer 2014 134(3), 575-86. Doramapimod (BIRB 796) purchased from Selleck.

  • A p38α/ERK crosstalk exists in CRC cells and tissues. Use of a structurally and functionally different p38α inhibitor (BIRB-796) confirms ERK1/2 phospho-activation. Using BIRB-796 for up to 72 h triggers MEK-ERK1/2 signaling in HT-29 cells.

    Cancer Lett 2012 324(1), 98-108. Doramapimod (BIRB 796) purchased from Selleck.

    Inhibition of p38 MAPK activity prevents induction of autophagy by glucose. NIH 3T3 cells were incubated in KH medium without glucose in the presence of the p38 MAPK inhibitor BIRB796 (50 nM, middle panels). After 30 min, glucose (10 mM) and lysosomal inhibitors were added to the indicated samples and cells were further incubated for 2 h. Cell lysates were collected and processed for SDS/PAGE. LC3 levels were detected and actin served as a loading control. The values shown in the histograms represent means盨.D. from three independent experiments with the LC3-II levels normalized to actin and expressed as a percentage of the values of KH medium without glucose. *P<0.05. Glc, glucose; w/o, without.

    Biochem J 2014 449(2), 497-506. Doramapimod (BIRB 796) purchased from Selleck.

  • Doramapimod (BIRB 796) purchased from Selleck.

Purity & Quality Control

Choose Selective p38 MAPK Inhibitors

Biological Activity

Description Doramapimod (BIRB 796) is a pan-p38 MAPK inhibitor with IC50 of 38 nM, 65 nM, 200 nM and 520 nM for p38α/β/γ/δ in cell-free assays, and binds p38α with Kd of 0.1 nM in THP-1 cells, 330-fold greater selectivity versus JNK2, weak inhibition for c-RAF, Fyn and Lck, insignificant inhibition of ERK-1, SYK, IKK2.
Features The first p38 MAPK inhibitor to be tested in a phase III clinical trial.
p38α [1]
(Cell-free assay)
p38α [7]
0.1 nM(Kd) 38 nM
In vitro

BIRB 796 shows no significant inhibition to ERK-1, SYK, IKK2β, ZAP-70, EGF receptor kinase, HER2, protein kinase A (PKA), PKC, PKC-α, PKC-β (I and II) and PKC-γ. BIRB 796 greatly improves binding affinity by forming a hydrogen bond between the morpholine oxygen and the ATP-binding domain of p38α. BIRB 796 represents one of the most potent and slowest dissociating inhibitors against human p38 MAP kinase now known. [1] BIRB 796 potently inhibits c-Raf-1 and Jnk2α2 with IC50 of 1.4 and 0.1 nM, respectively. [2] BIRB796 also inhibits the activity and the activation of SAPK3/p38γ at a higher concentration than it does in p38α. BIRB796 blocks the stress-induced phosphorylation of the scaffold protein SAP97, which is a physiological substrate of SAPK3/p38γ. BIRB796 blocks JNK1/2 activation and activity in HEK293 cells, while not inhibits the activation and activity of ERK1/ERK2 in Hela cells. Moreover, the binding of BIRB796 to the p38 MAPKs or JNK1/2 is impairing their phosphorylation by the upstream kinase MKK6 or MKK4 rather than enhancing their dephosphorylation. [3] BIRB 796 blocks baseline and bortezomib-triggered upregulation of p38 MAPK and Hsp27 phosphorylation, thereby enhancing cytotoxicity and caspase activation. BIRB 796 downregulates IL-6 and VEGF secretion in BMSCs triggered by TNF-α and TGF-β1. [4] BIRB-796 has a pyrazole scaffold that places a lipophilic t-butyl group into the lower selectivity site and a tolyl ring into the upper selectivity site. BIRB-796 also inhibits B-Raf and Abl with IC50 of 83 nM and 14.6 μM, respectively. [5]

Cell Data
Cell Lines Assay Type Concentration Incubation Time Formulation Activity Description PMID
EoL-1-cell MYDHdo94fGhiSX7obYJqfGmxbjDBd5NigQ>? M{XiOmlEPTB;MD6zOFc3OyEQvF2= Mk\HV2FPT1KHUh?=
DU-145 NF\tR49Iem:5dHigTY5pcWKrdHnvckBCe3OjeR?= NVLab|VLUUN3ME2zMlk{QDFzIN88US=> NIHpN5ZUSU6JUlXS
NCI-H358 NHHiOpNIem:5dHigTY5pcWKrdHnvckBCe3OjeR?= NFfMZlhKSzVyPUeuOVM5KM7:TR?= NYjKZVUyW0GQR2LFVi=>
T-24 NIjGNplIem:5dHigTY5pcWKrdHnvckBCe3OjeR?= M2HGcmlEPTB;OD60NFY4OyEQvF2= NVTSb3BwW0GQR2LFVi=>
MPP-89 MorkS5Jwf3SqIFnubIljcXSrb36gRZN{[Xl? NFu4TFFKSzVyPUiuOFYzPTFizszN M2r3dnNCVkeURWK=
NCI-SNU-1 M3fSSWdzd3e2aDDJcohq[mm2aX;uJGF{e2G7 NVr0Z5hUUUN3ME25MlA3PzN7IN88US=> M1vk[XNCVkeURWK=
BFTC-905 Mk\2S5Jwf3SqIFnubIljcXSrb36gRZN{[Xl? NX;tUWdwUUN3ME2xNE4yOjN|IN88US=> MlTpV2FPT1KHUh?=
NBsusSR M4ruNGdzd3e2aDDJcohq[mm2aX;uJGF{e2G7 Mm\yTWM2OD1zMD64NlM2KM7:TR?= MkPYV2FPT1KHUh?=
BEN NHTvVm5Iem:5dHigTY5pcWKrdHnvckBCe3OjeR?= NXrBNHdRUUN3ME2xN{4yOjZ2IN88US=> NVTnXG5mW0GQR2LFVi=>
HMV-II NGnPfmZIem:5dHigTY5pcWKrdHnvckBCe3OjeR?= MkXYTWM2OD1zND6yN|A6KM7:TR?= NGi5TmlUSU6JUlXS
NCI-H1581 NVfXemIxT3Kxd4ToJGlvcGmkaYTpc44hSXO|YYm= MYPJR|UxRTF5LkC0OFch|ryP NXPPc5B{W0GQR2LFVi=>
ES8 NX3FS29YT3Kxd4ToJGlvcGmkaYTpc44hSXO|YYm= Mnn0TWM2OD1zNz6xOlch|ryP NGnjfpZUSU6JUlXS
LC-2-ad MYTHdo94fGhiSX7obYJqfGmxbjDBd5NigQ>? NHfEbYNKSzVyPUG3MlQ{PjZizszN MYHTRW5IWkWU
EW-13 MnzkS5Jwf3SqIFnubIljcXSrb36gRZN{[Xl? MnjYTWM2OD1zNz65OVE3KM7:TR?= MYnTRW5IWkWU
AN3-CA M{W3Z2dzd3e2aDDJcohq[mm2aX;uJGF{e2G7 MnvBTWM2OD1zOD6xJO69VQ>? Mn;oV2FPT1KHUh?=
DB NHztSo1Iem:5dHigTY5pcWKrdHnvckBCe3OjeR?= MVrJR|UxRTF6Lke5NlMh|ryP Mn\5V2FPT1KHUh?=
SK-MEL-1 MXPHdo94fGhiSX7obYJqfGmxbjDBd5NigQ>? MWXJR|UxRTJyLkO2PFMh|ryP M3frT3NCVkeURWK=
HOP-92 NEjtd2dIem:5dHigTY5pcWKrdHnvckBCe3OjeR?= NIDRNotKSzVyPUK0MlM5OzhizszN MnfEV2FPT1KHUh?=
KYSE-270 MXrHdo94fGhiSX7obYJqfGmxbjDBd5NigQ>? NYjIS5F7UUN3ME2yOE42PTd|IN88US=> M13IcnNCVkeURWK=
HCC1806 MXHHdo94fGhiSX7obYJqfGmxbjDBd5NigQ>? M2nFd2lEPTB;MkSuO|c6QSEQvF2= Mm[xV2FPT1KHUh?=
HuO-3N1 NGrkfZRIem:5dHigTY5pcWKrdHnvckBCe3OjeR?= MmP3TWM2OD1{NT64NVg2KM7:TR?= NYLkfItXW0GQR2LFVi=>
HOS MlfXS5Jwf3SqIFnubIljcXSrb36gRZN{[Xl? NWXnToZjUUN3ME2yOU46Ojl{IN88US=> M2myNnNCVkeURWK=
KYSE-510 MoHOS5Jwf3SqIFnubIljcXSrb36gRZN{[Xl? MmHnTWM2OD1{Nj6xOlEzKM7:TR?= NIjlbIVUSU6JUlXS
COLO-741 NHPNcllIem:5dHigTY5pcWKrdHnvckBCe3OjeR?= MlLVTWM2OD1{Nj6zN|I6KM7:TR?= M3W4eHNCVkeURWK=
H-EMC-SS MWLHdo94fGhiSX7obYJqfGmxbjDBd5NigQ>? NWnHdnZ6UUN3ME2yOk46OjR3IN88US=> Mn;NV2FPT1KHUh?=
HCC1937 NHvrXI9Iem:5dHigTY5pcWKrdHnvckBCe3OjeR?= NHWzOYRKSzVyPUK3MlIzOzhizszN NX\ROmhLW0GQR2LFVi=>
NCI-H2126 M4rpOWdzd3e2aDDJcohq[mm2aX;uJGF{e2G7 NIfXeGhKSzVyPUK3MlM6PzVizszN M4rzZXNCVkeURWK=
NCI-H1703 Ml;WS5Jwf3SqIFnubIljcXSrb36gRZN{[Xl? M4DzZ2lEPTB;MkiuNFQyOyEQvF2= MkjYV2FPT1KHUh?=
U-2-OS Mnz3S5Jwf3SqIFnubIljcXSrb36gRZN{[Xl? M1XQemlEPTB;MkiuOVUyPSEQvF2= M4jpUnNCVkeURWK=
DBTRG-05MG NHjl[odIem:5dHigTY5pcWKrdHnvckBCe3OjeR?= M1XzUGlEPTB;MkiuOVY2OSEQvF2= M4PZRnNCVkeURWK=
HCC1419 MojOS5Jwf3SqIFnubIljcXSrb36gRZN{[Xl? Mk\tTWM2OD1|Mj6xNVE6KM7:TR?= NIraSnRUSU6JUlXS
AM-38 M2riT2dzd3e2aDDJcohq[mm2aX;uJGF{e2G7 MY\JR|UxRTN{Lkm5N|Eh|ryP MkDWV2FPT1KHUh?=
NCI-H2009 MnP3S5Jwf3SqIFnubIljcXSrb36gRZN{[Xl? NH7Tc49KSzVyPUOzMlQxODdizszN MW\TRW5IWkWU
EM-2 Ml\pS5Jwf3SqIFnubIljcXSrb36gRZN{[Xl? MYnJR|UxRTN|LkW1NVEh|ryP MYnTRW5IWkWU
SW1116 M3vVV2dzd3e2aDDJcohq[mm2aX;uJGF{e2G7 NXrGWYFlUUN3ME2zOE41QDN6IN88US=> MUDTRW5IWkWU
SK-N-AS Mm\4S5Jwf3SqIFnubIljcXSrb36gRZN{[Xl? NYXEOoNCUUN3ME2zOU4xPzF2IN88US=> MoXiV2FPT1KHUh?=
ChaGo-K-1 M12xbWdzd3e2aDDJcohq[mm2aX;uJGF{e2G7 NGXxWXNKSzVyPUO1MlYxOzJizszN M3HHTHNCVkeURWK=
RT-112 MWXHdo94fGhiSX7obYJqfGmxbjDBd5NigQ>? MW\JR|UxRTN3Lkm4O|kh|ryP M1uxOHNCVkeURWK=
HTC-C3 MV3Hdo94fGhiSX7obYJqfGmxbjDBd5NigQ>? Ml65TWM2OD1|Nj6yN|U2KM7:TR?= MnmzV2FPT1KHUh?=
LB831-BLC Mn3sS5Jwf3SqIFnubIljcXSrb36gRZN{[Xl? MXLJR|UxRTN5Lk[1OFEh|ryP MVjTRW5IWkWU
MOLT-4 MYfHdo94fGhiSX7obYJqfGmxbjDBd5NigQ>? NYfhPHdCUUN3ME2zPE45OzlzIN88US=> NHT1RWxUSU6JUlXS
SW756 MV\Hdo94fGhiSX7obYJqfGmxbjDBd5NigQ>? NEXMdYpKSzVyPUSwMlk{QDVizszN MojYV2FPT1KHUh?=
KNS-62 MoTmS5Jwf3SqIFnubIljcXSrb36gRZN{[Xl? MoTxTWM2OD12Mj62Nlk3KM7:TR?= NVnDWZFlW0GQR2LFVi=>
KARPAS-299 MoPoS5Jwf3SqIFnubIljcXSrb36gRZN{[Xl? NHrYZVdKSzVyPUSzMlMzOzNizszN NWG0XlBtW0GQR2LFVi=>
KP-4 NYHidYR1T3Kxd4ToJGlvcGmkaYTpc44hSXO|YYm= NF30XohKSzVyPUS2Mlc{PjFizszN MYfTRW5IWkWU
G-402 MlHXS5Jwf3SqIFnubIljcXSrb36gRZN{[Xl? NIHJ[mdKSzVyPUS4MlcxOTJizszN M{\JXnNCVkeURWK=

... Click to View More Cell Line Experimental Data

In vivo BIRB 796 (30 mg/kg) inhibits 84% of TNF-α in LPS-stimulated mice and demonstrates efficacy in a mouse model of established collagen-induced arthritis. [1] BIRB 796 has good pharmacokinetic performance even after oral administration in mice. [2]


Animal Research:


+ Expand
  • Animal Models: Collagen-induced arthritis in female Balb/c mice
  • Formulation: 70% PEG400 (intravenous) or 100% PEG400 (oral)
  • Dosages: 1 mg/kg (intravenous) or 10 mg/kg (oral)
  • Administration: Intravenous injection or by oral
    (Only for Reference)

Solubility (25°C)

In vitro DMSO 100 mg/mL (189.51 mM)
Ethanol 100 mg/mL (189.51 mM)
Water Insoluble
In vivo Add solvents to the product individually and in order(Data is from Selleck tests instead of citations):
30% PEG400+0.5% Tween80+5% propylene glycol
For best results, use promptly after mixing.
30 mg/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 527.66


CAS No. 285983-48-4
Storage powder
in solvent
Synonyms N/A

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Clinical Trial Information

NCT Number Recruitment Conditions Sponsor/Collaborators Start Date Phases
NCT02214888 Terminated Arthritis Rheumatoid Boehringer Ingelheim May 2003 Phase 2
NCT02214888 Terminated Arthritis Rheumatoid Boehringer Ingelheim May 2003 Phase 2
NCT02211885 Completed Healthy Boehringer Ingelheim October 2002 Phase 1
NCT02211885 Completed Healthy Boehringer Ingelheim October 2002 Phase 1
NCT02209753 Completed Psoriasis Boehringer Ingelheim June 2001 Phase 2
NCT02209753 Completed Psoriasis Boehringer Ingelheim June 2001 Phase 2

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p38 MAPK Signaling Pathway Map

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Cell Lines Assay Type Concentration Incubation Time Formulation Activity Description PMID