PD169316, a p38 MAPK inhibitor. When at 5 μM or higher,it can block TGFβ signaling activity and thus caution must be used when attributing cellular activities exclusively to p38 MAPK signaling when these inhibitors are used experimentally. PD169316 attenuated apoptosis in potassium-deprived cells in a dose dependent manner significantly . PD169316 rescued the inhibitory effect of sphingosine on the formation of inositol phosphates by PGF(2alpha) or NaF in osteoblast-like MC3T3-E1 cells.
|Body Surface Area (m2)||0.007||0.025||0.15||0.05||0.02||0.5|
|Animal A (mg/kg) = Animal B (mg/kg) multiplied by||Animal B Km|
|Animal A Km|
For example, to modify the dose of resveratrol used for a mouse (22.4 mg/kg) to a dose based on the BSA for a rat, multiply 22.4 mg/kg by the Km factor for a mouse and then divide by the Km factor for a rat. This calculation results in a rat equivalent dose for resveratrol of 11.2 mg/kg.
|Solubility||DMSO 10 mg/mL|
The p38 MAPK inhibitor, PD169316, inhibits transforming growth factor beta-induced Smad signaling in human ovarian cancer cells.
Fu Y, et al. Biochem Biophys Res Commun. 2003 Oct 17;310(2):391-7. PMID: 14521923.
Inhibition of p38 kinase mimics survival signal-linked protection against apoptosis in rat cerebellar granule neurons.
Nath R, et al. Cell Mol Biol Lett. 2001;6(2):173-84. PMID: 11544639.
|Related p38 MAPK Products|
TA-02 is a p38 MAPK inhibitor with IC50 of 20 nM. IC50 value: 20 nM. TA-02 is a novel compound with similar cardiogenic properties as SB203580 and SB202190. TA-02 especially inhibits TGFBR-2.
Pexmetinib (ARRY-614) is a potent, orally bioavailable, dual p38 MAPK/Tie-2 inhibitor with IC50 of 4 nM/18 nM in a HEK-293 cell line. Phase 1.
Losmapimod (GW856553) is a selective, potent, and orally active p38 MAPK inhibitor with pKi of 8.1 and 7.6 for p38α and p38β, respectively.
VX-745 is a potent and selective inhibitor of p38α with IC50 of 10 nM, 22-fold greater selectivity versus p38β and no inhibition to p38γ.
TAK-715 is a p38 MAPK inhibitor for p38α with IC50 of 7.1 nM, 28-fold more selective for p38α over p38β, no inhibition to p38γ/δ, JNK1, ERK1, IKKβ, MEKK1 or TAK1.
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