Biological Activity

Bioactivity / Mechanism

In PDAC cell lines with high basal phospho-STAT3, AZ960 (1 µM, 24 h) reduced STAT3 Tyr705 phosphorylation and Bcl-xL expression. STAT3 Ser727 phosphorylation was unaffected. These cellular findings support pathway modulation without establishing biochemical JAK2 selectivity. [1]

Literature-reported observations and conditions; not Adooq-tested protocols or general treatment recommendations.

Target & Activity

Target	Activity	Value
JAK2	Ki	0.45 nM
JAK2		<3 nM

Cellular Effect

Cell Line	Activity	Value	Description	Reference
SET-2	GI50	0.033 μM	Growth inhibition of human SET2 cells expressing JAK2 V617F mutant after 48 hrs by alamar blue assay	[PMID: 21493067]

In Vitro Studies

AZ960 (1 µM, 72 h) increased Annexin V-positive cells in the phospho-STAT3-high PDAC lines MIAPACA2 and KP-4. The low-phospho-STAT3 lines Suit2 and ASPC1 did not show the corresponding apoptosis response or reductions in phospho-STAT3 and Bcl-xL, indicating a cell-context-dependent response. [1]

Context-dependent STAT3 signaling and apoptosis response in PDAC cells

Cell-based study · Human PDAC cell lines MIAPACA2 and KP-4 (high basal P-STAT3) versus Suit2 and ASPC1 (low basal P-STAT3) [1]

At 1 µM AZ960, high-P-STAT3 cells showed reduced Tyr705-phosphorylated STAT3 and Bcl-xL at 24 h and increased Annexin V positivity at 72 h. Low-P-STAT3 lines lacked the corresponding response. Ser727-phosphorylated STAT3 was unaffected.

Measured endpoints — not treatment concentrations
Endpoint	Reported result	Reference
STAT3 Tyr705 and Ser727 phosphorylation; total STAT3 and Bcl-xL protein	Immunoblot response Reduced P-Tyr705-STAT3 and Bcl-xL in MIAPACA2/KP-4; no corresponding reduction in Suit2/ASPC1. P-Ser727-STAT3 unaffected.	[1]
Annexin V-positive cells	Apoptosis response Increased in MIAPACA2 and KP-4; low-P-STAT3 Suit2 and ASPC1 did not show corresponding induction. Caption marks **p < 0.01 for the responsive lines. No exact percentages estimated.	[1]

Literature-Reported Treatment Conditions

Treatment concentration: 1 µM
Exposure duration: 24 h for immunoblot; 72 h for Annexin V endpoint
Method: Single-compound cell treatment; separate endpoint sampling times
Reported limits: AZ960 supplier, salt, lot, enantiopurity and solvent not specified in inspected main-text chemical methods/caption. Figure 1D replicate count, error-bar definition and statistical test are not specified there; do not transfer triplicate/SD wording from Figure 1C. Supplementary document not retrieved.

Methods and source locations

Compound reported in the paper: AZ960

Named AZ960 cellular experiment only; no Adooq lot validation, direct target-binding or biochemical-selectivity conclusion.

Figure 1D and caption; Results first subsection, P13; Materials and Methods, Cell Lines (P6) and Molecular Analyses (P9)

STAT3 Tyr705 and Ser727 phosphorylation; total STAT3 and Bcl-xL protein: Immunoblot after 24 h with or without 1 µM AZ960; total STAT3 and β-actin bands included. — Figure 1D left and caption; Results P13; Molecular Analyses P9

Annexin V-positive cells: 72 h with or without 1 µM AZ960; Annexin V staining. Cell Lines methods describe Annexin V Cy5/propidium iodide flow cytometry. — Figure 1D right and caption; Results P13; Cell Lines P6

In Vivo Studies

In male NC/Nga mice with Dermatophagoides farinae extract-induced atopic dermatitis, oral AZ960 (1.58 mg/kg, one dose per week for three weeks) did not significantly suppress mechanical alloknesis or spontaneous scratching compared with vehicle. This result is specific to the tested model and intermittent schedule. [2]

No significant suppression of itch behaviors in an atopic dermatitis mouse model

Animal study · Male NC/Nga mice, 8–10 weeks old, with D. farinae extract-induced atopic dermatitis; n = 8 per group [2]

In male NC/Nga mice with Dermatophagoides farinae extract-induced atopic dermatitis, oral AZ960 (1.58 mg/kg, one dose per week for three weeks) did not significantly suppress mechanical alloknesis or spontaneous scratching compared with vehicle. This result is specific to the tested model and intermittent schedule.

Measured endpoints — not treatment concentrations
Endpoint	Reported result	Reference
Mechanical alloknesis scores with 0.07 g and 0.16 g von Frey stimuli; spontaneous scratching bouts over 2 h	Behavioral response No significant suppression versus vehicle; n = 8 per group; plotted data mean ± SEM	[2]

Conditions shared by the study groups

Route: Oral
Frequency: A single dose each week
Treatment course: Three weeks; assessments at weeks 1, 2 and 3
Vehicle: 2.5% DMSO in methyl cellulose solution

Study groups and reported outcomes
Group / dose	Comparator	Observed result	Reference
AZ960 in AD mice 1.58 mg/kg	Vehicle-treated AD mice; abrocitinib and baricitinib were pharmacological comparators in the same experiment	No significant suppression of mechanical alloknesis or spontaneous scratching versus vehicle.	[2]

AZ960 in AD mice: Model: Male NC/Nga mice, 8–10 weeks old, with D. farinae extract-induced atopic dermatitis; n = 8 per group; Reported limits: Exact numeric group means and AZ960-specific p values were not tabulated in the inspected material. Exact post-dose interval for the alloknesis assessment and methyl cellulose concentration were not specified in the relevant text.

Methods and source locations

Compound reported in the paper: AZ960

Limited to the named AZ960 treatment in this mouse study; no claim of Adooq validation or demonstrated JAK2 target engagement.

Sections 2.1, 2.3–2.5 and 3.2; Figure 1a and Figure 4a–c with captions; Discussion paragraph on assessment timing

Mechanical alloknesis scores with 0.07 g and 0.16 g von Frey stimuli; spontaneous scratching bouts over 2 h: Mechanical alloknesis score: scratching responses to 30 mechanical stimuli. Spontaneous scratching recorded with SCLABA-Next. — Section 2.4, Section 3.2 and Figure 4a–c caption

AZ960 in AD mice · Sections 2.1, 2.3–2.5 and 3.2; Figure 1a and Figure 4a–c with captions; Discussion paragraph on assessment timing

Specifications

Manufacturer	Adooq Bioscience
Actions	Inhibitor
CAS Number	905586-69-8
Applications	JAK2 inhibitor
Formula	C₁₈H₁₆F₂N₆
Molecular Weight	354.4
SMILES	CC1=CC(=NN1)NC2=C(C=C(C(=N2)N[C@@H](C)C3=CC=C(C=C3)F)C#N)F

Storage & Solubility

In Vitro Solubility

Reported Solubility

Solvent	Reported Solubility
DMSO	70 mg/mL (197.54 mM)
Water	Insoluble
Ethanol	3 mg/mL (8.46 mM)

Preparing Stock Solutions

Stock preparation is unavailable for this product molecular weight.

Calculated stock concentrations do not establish solvent solubility. Refer to the reported solubility data for experimental guidance.

Storage

Store powder at -20°C, keep desiccated.
In powder form, the chemical is stable for 36 months.
In solution, store at -20°C and use within 1 month to prevent loss of potency. Aliquot to avoid multiple freeze/thaw cycles.

Research References

[1] Corcoran RB, Contino G, Deshpande V, et al. STAT3 plays a critical role in KRAS-induced pancreatic tumorigenesis Cancer Research (2011). PMID: 21586612 DOI: 10.1158/0008-5472.CAN-11-0908 Source material
[2] Zuo Y, Toyama S, Morita M, et al. JAK1 Signaling Is Involved in the Induction of Mechanical Alloknesis in Atopic Dermatitis. Biomedicines (2025). PMID: 41301837 DOI: 10.3390/biomedicines13112744 Source material

Publications

1 publication citing this product

Rongshou Wu, .et al. , Sci Rep, 2023, 13: 16998 PMID: 37813900

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AZ-960

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AZ-960 1 mg

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