country

Change Language

EN - English
FR - Français
DE - Deutsch
ES - Español
JA - 日本語
KO - 한국어

Country or Region:

United States

Product Name	Size / Unit Price	Qty

Total: USD 0.00 Checkout

Cat. No.: HY-184412

Copy Link Print Information

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.

Nos produits utilisent uniquement pour la recherche. Nous ne vendons pas aux patients.

Formule: C₂₄H₂₄ClN₃O₂S
Masse moléculaire:453.98

Stockage:

Please store the product under the recommended conditions in the Certificate of Analysis.

SDUY104 Chemical Structure

Size

Prix

Stock

Quantité

Amount: USD 0.00

* Veuillez sélectionner la quantité avant d'ajouter des articles.

Top Publications Citing

Use of MCE Products

Fluorescent Dye

Strong Fluorescence Signal / Multi-Disciplinary Applications / High Fluorescence Specificity

Activité biologique
- Description
- IC₅₀ & Target
- Cellular Effect
- In Vitro
- Parmacokinetics
- In Vivo
Chemical Information
Pureté et documentation
Références
Calculators
Help & FAQs
Classifications
Bioz

Activité biologique

Description

IC₅₀ & Target^[1]

SHP2

140 nM (IC₅₀)

p38 MAPK

Voir tous les produits spécifiques à Isoform p38 MAPK :

Cellular Effect

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

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	T_max	C_max	T_1/2	AUC	CL	V_ss	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 (HY-15816) or Buparlisib (BKM-120) (HY-70063), 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, K_i67 and TUNEL staining.

Chemical Information

Masse moléculaire 453.98
Formule C₂₄H₂₄ClN₃O₂S
SMILES

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

Room temperature in continental US; may vary elsewhere.
Stockage

Please store the product under the recommended conditions in the Certificate of Analysis.

Pureté et documentation

Instruction de manipulation (2659 KB)

Références

[1]. Zhu C, et al. SHP2 Inhibition Reveals Compensatory PI3K-AKT Activation in KRAS-Driven Pancreatic Cancer: Discovery of SDUY104 and Rational Approaches for Combination Therapy. J Med Chem. 2026 Jun 25;69(12):14774-14803. [Content Brief]

Calculators

Calculateur de molarité

Mass (g) = Concentration (mol/L) × Volume (L) × Molecular Weight (g/mol)

Mass Mass

Concentration Concentration

Volume Volume

Molecular Weight Molecular Weight

Calculateur de dilution

Concentration _(start) × Volume _(start) = Concentration _(final) × Volume _(final)

Concentration _(start) Concentration _(start)

Volume _(start) Volume _(start)

Concentration _(final) Concentration _(final)

Volume _(final) Volume _(final)

Help & FAQs

How should lyophilized recombinant proteins be reconstituted and stored?

1. Before opening the cap, centrifuge the vial at 13000 rpm for 20-30 seconds. This step will ensure that any lyophilized powder that may have adhered to the cap or walls is collected at the bottom of the vial, minimizing the risk of product loss.

MOQ

Minimum order quantity

100 mg

Obtenir un devis En stock

Other size

Obtenir un devis

Amount: USD 0.00

Activité biologique
- Description
- IC₅₀ & Target
- In Vitro
- In Vivo
Chemical Information
Pureté et documentation
Références

Nom du produit:
Cat. No.:
Quantité:
MCE Japan Authorized Agent:

Nom du produit:
CAS No.:
Species:
Pureté:
Quantité:

SDUY104

Voir tous les produits spécifiques à Isoform p38 MAPK

Activité biologique

Chemical Information

Pureté et documentation

Références

Calculators

Help & FAQs

SDUY104 Related Classifications

HY-184412 Related Classifications