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p38 MAP Kinase Inhibitor - InvitroFit™

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5 x 5 mg

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p38 MAP Kinase Inhibitor

p38 MAP Kinase inhibition by SB203580
p38 MAP Kinase inhibition by SB203580

SB203580 is a pyridinyl imidazole inhibitor widely used to study the role of p38 mitogen-activated protein (MAP) kinase [1]. The p38 MAP kinase signaling pathway allows cells to interpret a wide range of external signals and respond appropriately by generating a plethora of different biological effects.

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Mode of action:

SB203580 inhibits p38 catalytic activity by binding to the ATP binding pocket. It also inhibits the phosphorylation and activation of protein kinase B (PKB, also known as Akt) [2]. Both kinases are involved in a wide array of signaling pathways, including the Toll-like receptor (TLR) signaling pathway [3].

Moreover, several studies suggest that p38 MAPKs regulate distinct phases of autophagy. p38 can elicit autophagy via Beclin-1. Contrarily, p38α has also been reported to inhibit autophagy by interfering with the trafficking of Atg9.
SB203580 is generally used at low concentrations (1-10 μM), as it has been reported that at high concentrations (>20 μM) SB203580 can induce the activation of the serine/threonine kinase Raf-1 [4].


Key features:

  • p38 MAP Kinase inhibitor - Autophagy inducer
  • InvitroFit™ grade: each lot is highly pure (≥98%) and functionally tested



1. Cuenda A. et al., 1995. SB203580 is a specific inhibitor of a MAP kinase homologue which is stimulated by cellular stresses and interleukin-1. FEBS Lett. 364:229-233.
2. Lali FV. et al., 2000. The pyridinyl imidazole inhibitor SB203580 blocks phosphoinositide-dependent protein kinase activity, protein kinase B phosphorylation, and retinoblastoma hyperphosphorylation in interleukin-2-stimulated T cells independently of p38 mitogen-activated protein kinase. J Biol Chem. 275(10):7395-402.
3. Jarnicki A.G. et al., 2008. Attenuating regulatory T cell induction by TLR agonists through inhibition of p38 MAPK signaling in dendritic cells enhances their efficacy as vaccine adjuvants and cancer immunotherapeutics. J. Immunol., 180: 3797-3806.
4. Kalmes A et al., 1999. Raf-1 is activated by the p38 mitogen-activated protein kinase inhibitor, SB203580. FEBS Lett. 444(1):71-4.


Dose-dependent inhibition of p38 MAP kinase signaling
Dose-dependent inhibition of p38 MAP kinase signaling

SB203580 is a potent inhibitor of p38 MAP kinase signaling.
RAW-Lucia™ ISG cells were incubated overnight at 37°C in the presence of increasing concentrations of SB203580 together with 100 ng/ml of LPS‑EB. The next day, the inhibitory activity of SB203580 was determined by measuring the reduction of Lucia luciferase production in the supernatant using the QUANTI‑Luc™ detection reagent. Data are shown as percentage (%) inhibition ± standard error of the mean (SEM).

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Working concentration: 1-10 μM

CAS number: 152121-47-6

Solubility: DMSO (50 mg/ml)

Synonym: 4-(4’-Fluorophenyl)-2-(4’-methylsulfinylphenyl)-5- (4’-pyridyl)-imidazole

Molecular weight: 377.44 g/mol

Formula: C6H16FN3OS

Quality control:

  • Purity ≥ 98% (UHPLC)
  • The inhibitory activity has been validated using cellular assays.
  • The absence of bacterial contamination (e.g. lipoproteins and endotoxins) has been confirmed using HEK-Blue™ TLR2 and HEK-Blue™ TLR4 cells.
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SB203580 is provided as a translucent film.

  • 5 mg

SB203580 is and shipped at room temperature.

Store at -20°C in the dark.

Solid product is stable 1 year at -20°C.

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p38 MAP Kinase

Mitogen-activated protein kinase (MAPK) pathway is an intracellular signal transduction pathway that regulates a plethora of cellular processes, including cell growth, cell proliferation, cell differentiation, stress response, migration, and apoptosis, in response to various extracellular stimuli [1, 2]. It consists of three pathways that involve extracellular-signal-regulated kinase 1 and 2 (ERK1/2), c-Jun N-terminal kinase 1, 2, and 3 (JNK1/2/3), and p38 MAPK signaling pathways [3]. ERK1/2 is activated in response to growth factors, hormones, and proinflammatory stimuli, while JNK1/2/3 and p38 MAPKs are activated by cellular and environmental stresses, in addition to pro-inflammatory stimuli.
p38 MAPKs are responsive to stress stimuli, such as cytokines, ultraviolet irradiation, heat shock, and osmotic shock, and are involved in cell differentiation, apoptosis, and autophagy. Persistent activation of the p38 MAPK pathway in muscle stem cells due to aging impairs muscle regeneration. Of note,  four p38 MAP kinases, p38-α (MAPK14), -β (MAPK11), -γ (MAPK12 / ERK6), and -δ (MAPK13 / SAPK4), have been identified.



1. Pua L.J.W. et al., 2022. Functional Roles of JNK and p38 MAPK Signaling in Nasopharyngeal Carcinoma. Int J Mol Sci. 23(3):1108.
2. Cuadrado A. & Nebreda A.R., 2010. Mechanisms and functions of p38 MAPK signalling. Biochem J. 429(3):403-17.
3. Zhang W. & Liu H.T., 2002. MAPK signal pathways in the regulation of cell proliferation in mammalian cells. Cell Res. 12:9–18.


SB203580 chemical properties

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