2. Protein Tyrosine Kinase/RTK Apoptosis MAPK/ERK Pathway
  3. SHP2 Apoptosis p38 MAPK
  4. SDUY104

SDUY104 is an orally active amide-based allosteric inhibitor of SHP2 with an IC50 of 140 nM. SDUY104 impairs KRAS-driven pancreatic cancer cell proliferation via cell-cycle arrest and apoptosis. SDUY104 suppresses MAPK signaling and triggers compensatory PI3K–AKT activation. SDUY104 can be used for KRAS-mutant pancreatic cancer research.

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SDUY104

SDUY104 Chemical Structure

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SDUY104 Related Antibodies

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p38 MAPK Akt1 p38α p38β MAPK13 p38δ p38γ

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Description

SDUY104 is an orally active amide-based allosteric inhibitor of SHP2 with an IC50 of 140 nM. SDUY104 impairs KRAS-driven pancreatic cancer cell proliferation via cell-cycle arrest and apoptosis. SDUY104 suppresses MAPK signaling and triggers compensatory PI3K–AKT activation. SDUY104 can be used for KRAS-mutant pancreatic cancer research[1].

IC50 & Target[1]

SHP2

140 nM (IC50)

p38 MAPK

 

Cellular Effect
Cell Line Type Value Description References
BXPC-3 IC50
61 μM
Inhibited the growth of BXPC-3 cells for 48 h.
Inhibited the growth of BXPC-3 cells for 48 h.
42261691
Panc02 IC50
63 μM
Inhibited the growth of Panc02 cells for 48 h.
Inhibited the growth of Panc02 cells for 48 h.
42261691
CAPAN-1 IC50
64 μM
Inhibited the growth of CAPAN-1 cells for 48 h.
Inhibited the growth of CAPAN-1 cells for 48 h.
42261691
PANC-1 IC50
38 μM
Inhibited the growth of PANC-1 cells for 48 hours.
Inhibited the growth of PANC-1 cells for 48 hours.
42261691
SW1990 IC50
73 μM
Inhibited the growth of SW1990 cells for 48 hours.
Inhibited the growth of SW1990 cells for 48 hours.
42261691
Hs 766 IC50
43 μM
Inhibited Hs 766 cell growth for 48 hours.
Inhibited Hs 766 cell growth for 48 hours.
42261691
MIA PaCa-2 IC50
55 μM
Inhibited MIA PaCa-2 cells growth for 48 hours.
Inhibited MIA PaCa-2 cells growth for 48 hours.
42261691
Panc203 IC50
85 μM
Inhibited Panc203 cells growth for 48 hours.
Inhibited Panc203 cells growth for 48 hours.
42261691
In Vitro

SDUY104 binds to and competitively occupies the SHP2 tunnel allosteric pocket with an IC50 of 1.5 μM[1].
SDUY104 (10 μM; 30 min) markedly inhibits SHP2 enzymatic activity with an IC₅₀ of 140 nM[1].
SDUY104 (10 μM; 30 min) exhibits negligible inhibitory activity against other phosphatases (PTP1B, SHP1, TCPTP, LMWPTP) except SHP2[1].
SDUY104 (30 μM; 24 h) directly binds intracellular SHP2 and markedly stabilizes SHP2 against thermal denaturation in PDAC cells[1].
SDUY104 (48 h) elicits dose-dependent antiproliferative activity across KRAS mutant and wild-type PDAC cells with IC50s of 38-85 μM[1].
SDUY104 (30 μM; 24 h) induces G0/G1 arrest in BxPC-3 and PANC-1 cells[1].
SDUY104 (10-30 μM; 48 h) substantially induces late apoptosis in BxPC-3 cells while exhibiting minimal efficacy in PANC-1 cells at the same concentration[1].
SDUY104 (1-10 μM; 24-48 h) suppresses MAPK signaling but induces compensatory PI3K-AKT reactivation in BxPC-3 and PANC-1 cells[1].
SDUY104 (5 μM; 48 h) suppresses MAP signaling while paradoxically reactivates the PI3K-AKT pathway in PDAC cells via SHP2 inhibition[1].
SDUY104 (5-40 μM; 3 days) and Ulixertinib (HY-15816) act in combination to achieve synergistic suppression of PDAC cell proliferation[1].
SDUY104 (2-5 μM; 24 h) and Ulixertinib synergistically inhibit MAPK signaling in BxPC-3 and PANC-1 cells[1].
SDUY104 (30 μM; 72 h) exerts potentiated antiproliferative effects in BxPC-3 and PANC-1 cells in the presence of BKM-120 (HY-70063)[1].
SDUY104 (10 μM; 24 h) induces elevated AKT phosphorylation, and this effect is markedly counteracted by BKM-120 in both KRAS-mutant and wild-type cell lines[1].

MedChemExpress (MCE) has not independently confirmed the accuracy of these methods. They are for reference only.

SDUY104 Related Antibodies

Apoptosis Analysis[1]

Cell Line: BxPC-3 cells, PANC-1 cells
Concentration: 10 μM, 30 μM
Incubation Time: 48 h
Result: Robustly induced late-stage apoptosis in BxPC-3 cells while exhibiting weak effects in PANC-1 cells at the same concentration.

Cell Viability Assay[1]

Cell Line: BxPC-3 cells, PANC-1 cells
Concentration: 30 μM
Incubation Time: 24 h
Result: Induced G0/G1 cell cycle arrest, with stronger activity in BxPC-3 than PANC-1 cells.

Western Blot Analysis[1]

Cell Line: BxPC-3 cells, PANC-1 cells
Concentration: 1 μM, 3 μM, 10 μM
Incubation Time: 24 h, 48 h
Result: Dose-dependently inhibited ERK phosphorylation in BxPC-3 cells.
Dose-dependently inhibited ERK phosphorylation in KRAS mutant PANC-1 cells.
Significantly upregulated AKT phosphorylation in a dose-dependent manner in BxPC-3 and PANC-1 cells.

Apoptosis Analysis[1]

Cell Line: PDAC cells
Concentration: 5 μM, 10 μM, 20 μM, 30 μM, 40 μM
Incubation Time: 3 days
Result: Acted synergistically with Ulixertinib to inhibit PDAC cells proliferation.

Western Blot Analysis[1]

Cell Line: BxPC-3 cells, PANC-1 cells
Concentration: 2 μM, 5 μM
Incubation Time: 24 h
Result: Acted synergistically with Ulixertinib to decrease phosphorylated RSK levels in BxPC-3 and PANC-1 cells.

Cell Viability Assay[1]

Cell Line: BxPC-3 cells, PANC-1 cells
Concentration: 30 μM
Incubation Time: 72 h
Result: Induced 14% growth inhibition in BxPC-3 cells when used alone.
Reached a growth inhibition rate of 61% in BxPC-3 cells when co-administered with 100 nM BKM-120.
Yielded comparable synergistic antiproliferative effects in PANC-1 cells when combined with BKM-120.

Western Blot Analysis[1]

Cell Line: BxPC-3 cells, PANC-1 cells
Concentration: 10 μM
Incubation Time: 24 h
Result: Raised AKT phosphorylation to approximately 141.8% of control levels in BxPC-3 cells.
Triggered AKT phosphorylation was markedly lowered to 35.9% after co-treatment with 1 μM BKM-120 in BxPC-3 cells.
Elevated AKT phosphorylation to 155.2% relative to controls in PANC-1 cells.
Elevated AKT phosphorylation in PANC-1 cells, and 1 μM BKM-120 lowered this phosphorylated level to 21.7%.
Parmacokinetics
Species Dose Route Tmax Cmax T1/2 AUC CL Vss F
Mice[1] 1 mg/kg i.v. 0.083 h 357 ng/mL 0.712 h 367 μg·h/mL 3696 mL/h/kg 2886 mL/kg /
Mice[1] 10 mg/kg p.o. 0.7 h 34.7 ng/mL 3.64 h 145 ng·h/mL / / 5.44 %
In Vivo

SDUY104 (50 mg/kg; p.o.; once daily; for 4 weeks) as single-agent therapy suppresses PANC-1 tumor growth, generates stronger antitumor effects when combined with Ulixertinib or BKM-120, and exhibits no obvious toxic signs in mice[1].

MedChemExpress (MCE) has not independently confirmed the accuracy of these methods. They are for reference only.

Animal Model: 5-week female BALB/c nude mice were acclimated for 1 week, inoculated with PANC-1 cells suspension (1 × 107 cells), and dosed at 9 weeks old (3 weeks post-inoculation) [1]
Dosage: 50 mg/kg (with 50 mg/kg Ulixertinib or 15 mg/kg BKM-120)
Administration: p.o.; once daily; for 3-4 weeks
Result: Significantly suppressed tumor growth and reduced tumor volume, and its combination with Ulixertinib or BKM-120 yielded superior inhibitory effects.
Showed no significant body weight loss.
Significantly inhibited ERK phosphorylation by 68% but induced a 75% upregulation of AKT phosphorylation.
Further deepened MAPK pathway suppression when combined with Ulixertinib, while it effectively abolished AKT hyperphosphorylation upon coadministration with BKM-120.
Reduced cancer cell density and proliferation more potently when combined with Ulixertinib or BKM-120 than monotherapy, as verified by H&E, Ki67 and TUNEL staining.
Molecular Weight

453.98

Formula

C24H24ClN3O2S
SMILES

NC1=CC=CC(SC2=CC=C(O2)C(N3CCC4(CC5=C([C@H]4N)C=CC=C5)CC3)=O)=C1Cl
Shipping

Room temperature in continental US; may vary elsewhere.
Storage

Please store the product under the recommended conditions in the Certificate of Analysis.
Purity & Documentation
References
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SDUY104 Related Classifications

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Help & FAQs
  • Do most proteins show cross-species activity?

    Species cross-reactivity must be investigated individually for each product. Many human cytokines will produce a nice response in mouse cell lines, and many mouse proteins will show activity on human cells. Other proteins may have a lower specific activity when used in the opposite species.

Keywords:

SDUY104SDUY 104SDUY-104SHP2Apoptosisp38 MAPKSrc homology phosphatase 2PTPN11SHP2 inhibitorMAPKPI3K-AKTantitumor activitycell cycle arrestapoptosisKRAS-mutant pancreatic cancerUlixertinibBKM-120furanamide derivativesKRAS mutant PDAC cellsphosphatasesBKM-120 cellsBxPC-3 cellsAKT phosphorylationERK phosphorylationtumorInhibitorinhibitorinhibit

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