PiF
PiF is a fluorescent probe with high specificity for pancreatic β-cells (Ex/Em = 535 nm/565 nm), and its fluorescence signal increases significantly with elevated insulin concentrations in in vitro experiments. PiF enables visualization of rat and human islets transplanted via the portal vein in mouse livers with low liver background signals. The fluorine atom of PiF can be replaced by radioactive 18F to prepare a PET tracer. PiF can be used for research on type 1 diabetes.
For research use only. We do not sell to patients.
- CAS No.: 2688758-23-6
- Formula: C26H26F4N2O5S
- Molecular Weight:554.55
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Storage:
Please store the product under the recommended conditions in the Certificate of Analysis.
To place orders, for customer services and technical support, please contact: MedChemExpress USA
Tel: 609-228-6898 E-mail: [email protected] [email protected]
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Biological Activity
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Chemical Information
- Protocols
- Purity & Documentation
- References
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Help & FAQs
Biological Activity
Description
In Vitro
PiF (0.5 μM; 30 min) shows a dose-dependent fluorescence response to bovine insulin in a cell-free 20 mM HEPES buffer system (pH 7.4) after 30 min of incubation[1].
PiF (1 μM; 30 min) is highly selective for insulin over glucagon and human serum albumin in a cell-free 20 mM HEPES buffer system (pH 7.4) after 30 min of incubation[1].
PiF (1 μM; 1 h) selectively stains pancreatic β-cells (not α-cells) in isolated mouse islets after 1 h of incubation, as confirmed by co-staining with cell-specific markers and gene expression analysis of sorted cell populations[1].
PiF (0.25-2 μM; 1 h) selectively stains isolated rat islets in a concentration-dependent, non-toxic manner after 1 h of incubation, with a linear correlation between fluorescence intensity and probe concentration[1].
MedChemExpress (MCE) has not independently confirmed the accuracy of these methods. They are for reference only. Further protocols information, click here.
In Vivo
[18F]PiF (~7.4 MBq; intravenous injection; single administration), as the PET tracer form of PiF, selectively accumulates in pancreatic β-cells of healthy ICR mice, reaching a peak uptake of 16.1 %ID/g at 30 minutes post-injection, and its specific uptake is confirmed by blocking experiments[1].
Guidelines (The following is our recommended protocol, which serves only as a guideline and should be modified according to your specific needs).
Rapid Visualization of β Cells/Islets in Mouse Pancreatic Tissue
1. Reagent Preparation: Prepare PiF stock solution (dissolved in DMSO), and dilute it to 300 μM with PBS containing 2% BSA prior to use.
2. Procedure:
2.1 In Vivo Injection: Inject PiF working solution (300 μM, 250 μL) into mice via the tail vein.
2.2 Incubation and Tissue Harvest:
Incubate for 1 hour to allow the probe to circulate and specifically accumulate in pancreatic β cells.
Euthanize the mice and rapidly harvest the pancreatic tissue.
2.3 Tissue Freezing (No Fixation/Dehydration Required):
Place the freshly harvested pancreatic tissue directly into Tissue-Freezing Media (TFM/OCT) and freeze it on dry ice.
This optimized protocol skips the traditional steps of 4% paraformaldehyde fixation and 30% sucrose dehydration.
2.4 Sectioning:
Use a cryostat to cut the tissue into 20 μm-thick frozen sections and mount them on glass slides.
2.5 Direct Staining and Observation:
Place the TFM/OCT-covered sections directly under a fluorescence microscope and observe using a TRITC filter (Ex 535 nm / Em 565 nm). PiF-stained islets (core of β cells) show strong red fluorescence.
Optional Washing: To remove the background from the embedding medium, add PBS dropwise onto the sections for incubation/rinsing before observing the PiF-specific signal.
MedChemExpress (MCE) has not independently confirmed the accuracy of these methods. They are for reference only.
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Animal Model:C57BL/6[1]
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Dosage:300 μM
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Administration:i.v.; single 250 μL injection via tail vein
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Result:Showed over 5 times higher average fluorescence intensity in pancreases of control nondiabetic mice than in streptozotocin-treated diabetic mice.
Detected 3.4 times more PiF-stained islets in control mice (3803 total) than in diabetic mice (1116 total).
Demonstrated over 2 times higher average fluorescence intensity per islet in control mice than in diabetic mice.
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Animal Model:ICR[1]
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Dosage:~7.4 MBq
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Administration:i.v.; single injection
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Result:Showed an initial pancreatic uptake of 10.8 %ID/g.
Reached a maximum uptake of 16.1 %ID/g at 30 minutes post-injection.
Was gradually washed out from the pancreas over the subsequent 90 minutes.
Showed significantly reduced pancreatic radioactivity uptake in a blocking experiment with excess cold PiF, confirming target specificity.
Clinical Trial
| NCT Number | Sponsor | Condition | Start Date |
Phase
|
|---|---|---|---|---|
| NCT01329991 | Plexxikon| | 2011-05 | PHASE1 |
Chemical Information
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CAS No. 2688758-23-6
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Molecular Weight 554.55
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Formula C26H26F4N2O5S
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SMILES
COC1=C(C=C(C=C1C)C2=C3C=CC(C=C3OC4=C2C=CC(N(CCF)C)=C4)=N)C.O=S(C(F)(F)F)(O)=O
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Shipping
Room temperature in continental US; may vary elsewhere.
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Storage
Please store the product under the recommended conditions in the Certificate of Analysis.
Protocols
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Research Protocol for Endocrine Diseases
Endocrine diseases often arise from disrupted hormone production, hormone signaling, or target-tissue responsiveness; for diabetes-focused endocrine disease models, insulin signaling regulates glucose uptake, hepatic glucose output, lipid metabolism, and β-cell compensation. Type 2 diabetes develops through interacting defects in insulin resistance, β-cell dysfunction, adipose inflammation, hepatic glucose overproduction, altered incretin signaling, and ectopic lipid metabolism. A major unresolved question is whether endocrine dysfunction is driven primarily by target-tissue insulin resistance, intrinsic β-cell failure, immune/inflammatory stress, or combined multi-organ failure that differs by disease stage.
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Human Islet Cell Culture
The method of preserving islets in vitro, with purified reduced immunogenicity. The steps are islet isolation, islet cell purification, in vitro determination of islet function and islet cell culture.
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Research Protocol for Metabolic Diseases
AMP-activated protein kinase, AMPK, is a conserved cellular energy sensor that responds to reduced cellular energy status and coordinates metabolism by increasing ATP-generating catabolic pathways while suppressing ATP-consuming anabolic processes. In metabolic disease research, the AMPK pathway is experimentally relevant because it regulates hepatic lipid synthesis, fatty acid oxidation, glucose production, skeletal-muscle glucose disposal, mTORC1-linked biosynthesis, autophagy, mitochondrial homeostasis, and whole-body energy balance. The central pathway logic is that energy stress, metformin, exercise-like stimulation, or direct AMPK activators increase AMPKα Thr172 phosphorylation and downstream substrate phosphorylation, including ACC and RAPTOR. Phosphorylation of ACC suppresses lipogenesis and supports fatty acid oxidation, whereas phosphorylation of RAPTOR suppresses mTORC1 signaling and links cellular energy status to growth and protein synthesis control. The pathway is linked
Purity & Documentation
References
Calculators
Concentration (start) × Volume (start) = Concentration (final) × Volume (final)
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