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Fig. 1 · Structure
Cat. No.
A12876
CAS No.
1228445-38-2
Formula
C23H25N5O3S
Mol. Weight
451.54

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Pyrintegrin

Cat. No. A12876 CAS 1228445-38-2
Pyrintegrin is a cell-permeable small molecule that promotes human embryonic stem cell (hESC) survival by > 30-fold.

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Publications for Pyrintegrin

1 publication citing this product

  1. Zhen Li, .et al. , Discov Oncol, 2025, Oct 31;16(1):2000 PMID: 41171493
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Biological Activity

Bioactivity / Mechanism

Pyrintegrin has cellular β1-integrin-activating activity: in injured murine and human podocytes, treatment increased activation-epitope staining relative to injury alone. This functional evidence does not establish direct binding or exclusive target selectivity. [1]

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

In Vitro Studies

Pyrintegrin protected cultured podocytes from puromycin aminonucleoside-associated cytoskeletal damage. The apparent EC50 for the normalized F-actin protection endpoint was 0.79 μM; 1 μM cotreatment also preserved actin/focal-adhesion readouts under separate validation conditions. [1]

In human adipose stem/progenitor cells, 2 μM pyrintegrin enhanced lipid accumulation and PPARγ/C/EBPα expression in adipogenic induction medium. Pyrintegrin alone in growth medium did not induce the same adipogenic response. [2]

A contrasting response was reported in established TU212-R laryngeal carcinoma cells: pyrintegrin partially reversed FGL1-knockdown-associated reductions in viability signal and integrin β1 expression during cisplatin treatment. This combination experiment, with unspecified in-vitro solvent controls, does not support an anticancer benefit. [3]

Podocyte protection and active β1-integrin readouts

Cell-based study · Cultured murine podocytes; human podocytes for activation-epitope validation [1]

Pyrintegrin protected actin-fiber readouts in PAN-injured podocytes and increased activation-epitope staining relative to PAN alone. This is cellular functional evidence, without a direct integrin-binding or purified-target assay.

Measured endpoints — not treatment concentrations
EndpointReported resultReference
Protection of normalized F-actin fiber count per cell in PAN-injured murine podocytesApparent cellular EC50 0.79 μM (Figure 5 label); 0.8 μM (rounded Results text)[1]
F-actin fibers, vinculin spots and active β1-integrin staining relative to PAN aloneQualitative direction Higher with pyrintegrin cotreatment than PAN alone; no exact bar heights extracted[1]

Literature-Reported Treatment Conditions

Treatment concentration
Concentration series for apparent EC50; 1 μM for Figure 6B–D
Exposure duration
48 h
Method
Cotreatment in cultured podocytes; high-content fluorescence imaging
Vehicle
DMSO, 1% (Figure 6 caption)
Co-treatment
Puromycin aminonucleoside (PAN): 16 μg/ml for Figure 5 dose-response; 30 μg/ml for Figure 6 validation. Figure 5 normalization uses PAN alone and PAN plus mizoribine (MZR; 5 μg/ml).
Reported limits
Supplemental methods not retrieved. Figure 5 and Figure 6 use different PAN concentrations; their conditions are not interchangeable.
Methods and source locations

Compound reported in the paper: Pyrintegrin; Compound label in the paper: pyr

Apparent EC50 describes protection of a normalized F-actin endpoint, not integrin-binding potency. Cellular activation-epitope signals do not establish exclusive target selectivity. No supplier-lot validation.

Figure 5 (Pyrintegrin panel); Figure 6A–D and captions; Results: A Small Molecule Integrin-β1 Agonist Protects Podocytes from Injury; Concise Methods: Podocyte HCS Assay

Protection of normalized F-actin fiber count per cell in PAN-injured murine podocytes: Curve fit; PAN-alone and PAN+MZR responses set at 0% and 100%. Each plotted point is one well, 500–1000 cells per well. — Figure 5 (Pyrintegrin panel); Figure 6A–D and captions; Results: A Small Molecule Integrin-β1 Agonist Protects Podocytes from Injury; Concise Methods: Podocyte HCS Assay

F-actin fibers, vinculin spots and active β1-integrin staining relative to PAN alone: 9EG7 for murine active β1; 12G10 for human active β1. B: means±SEM from three replicate wells; C: means±SEM from four to five wells; D: medians±SEM as caption states, four to five wells; 500–1000 cells/well. Cells are not independent biological replicates. — Figure 6B–D and caption

Adipogenic enhancement requires an induction context

Cell-based study · Human adipose tissue-derived stem/progenitor cells (hASCs), passages 4–5 [2]

At 2 μM, pyrintegrin increased lipid accumulation and adipogenic-marker expression in adipogenesis induction medium (AIM). The pyrintegrin-only condition in DMEM did not reproduce the adipogenic response.

Measured endpoints — not treatment concentrations
EndpointReported resultReference
Lipid accumulation with pyrintegrin in AIM versus AIM alone and pyrintegrin in DMEMQualitative microscopy outcome More lipid accumulation with AIM + 2 μM pyrintegrin; pyrintegrin alone failed to induce adipogenesis[2]
PPARγ and C/EBPα mRNA expressionQualitative qRT-PCR direction Higher with AIM + pyrintegrin than AIM alone; pyrintegrin alone did not induce the marker response[2]

Literature-Reported Treatment Conditions

Treatment concentration
2 μM
Exposure duration
4 wk for lipid accumulation (Figure 1B); day 7 for PPARγ and C/EBPα mRNA (Figure 1C)
Method
Pyrintegrin in AIM compared with DMEM, AIM alone and DMEM plus pyrintegrin
Vehicle
DMSO; final percentage not specified in the reviewed differentiation methods
Co-treatment
AIM contains dexamethasone, insulin, IBMX and indomethacin. This is an enhancement in an induction cocktail.
Reported limits
Experiments described as triplicates; donor-level n is not specified for these panels. Conflicting Figure 1A dose ranking is not adopted.
Methods and source locations

Compound reported in the paper: Pyrintegrin; Compound label in the paper: Ptn

Supports induced differentiation in this culture context; pyrintegrin alone was ineffective. No claim that 2 μM is optimal and no general standalone adipogenesis claim.

Figure 1B,C and caption; Results: Pyrintegrin promotes adipogenic differentiation; Methods: Multi-lineage differentiation, Pyrintegrin treatment, Real Time qRT-PCR, Lipid staining

Lipid accumulation with pyrintegrin in AIM versus AIM alone and pyrintegrin in DMEM: LipidTOX neutral-lipid imaging at 4 wk; no image-derived percentage extracted. — Figure 1B and caption; Results first subsection

PPARγ and C/EBPα mRNA expression: Day 7; GAPDH normalization; caption reports mean±SD and *P<0.05; methods: one-way ANOVA with Bonferroni tests. No exact fold changes inferred. — Figure 1C and caption

Contrasting survival response in a laryngeal carcinoma model

Cell-based study · Established TU212-R human laryngeal carcinoma cells; FGL1-knockdown and corresponding control groups [3]

The paper reports that pyrintegrin partially reversed the decrease in CCK-8 signal and integrin β1 expression associated with FGL1 knockdown during cisplatin exposure. Pyrintegrin plus cisplatin also gave higher viability signal than cisplatin alone. These model-specific observations limit extrapolation of a protective phenotype to an anticancer effect.

Measured endpoints — not treatment concentrations
EndpointReported resultReference
CCK-8 optical density at 450 nm and integrin β1 immunoblot expressionReported comparative direction Pyrintegrin partially reversed the sh-FGL1-associated reductions under cisplatin; pyrintegrin + cisplatin exceeded cisplatin alone in CCK-8 signal[3]

Literature-Reported Treatment Conditions

Treatment concentration
1 μM pyrintegrin
Exposure duration
48 h pyrintegrin exposure in the treatment methods
Method
Drug cotreatment of established cells; CCK-8 and immunoblot readouts
Vehicle
In-vitro pyrintegrin vehicle and final solvent fraction not specified in the reviewed treatment methods
Co-treatment
Cisplatin (CDDP; 8 μM for CDDP-containing treatment groups) and FGL1 knockdown; comparisons include CDDP alone and sh-FGL1-NC + CDDP.
Reported limits
Figure 2 does not resolve all CCK-8 timing details against the broader 24–72 h methods. No matched solvent-only control is identified in this figure. No survival fraction or proliferation rate inferred from optical density.
Methods and source locations

Compound reported in the paper: Pyrintegrin; Compound label in the paper: Pyrintegrin

An established tumor-cell rescue experiment under cisplatin exposure; not evidence of therapeutic benefit, target specificity or a general effect across cancers. Unspecified solvent controls limit causal attribution.

Figure 2B–D and caption; Methods treatment-group paragraphs, CCK-8 assay, Western blot and Statistical analysis; Results: Integrinβ1 is a functional mediator of CDDP resistance regulated by FGL1

CCK-8 optical density at 450 nm and integrin β1 immunoblot expression: Figure 2 caption n=3; immunoblots normalized to GAPDH; Methods report mean±SD, one-way ANOVA/Tukey for multiple groups. No numerical bar heights extracted. — Figure 2B–D and caption; Results corresponding subsection

In Vivo Studies

Locally implanted pyrintegrin-loaded collagen/PCL scaffolds increased lipid-positive tissue and mouse PPARγ expression after 4 weeks in the inguinal fat pad of C57BL/6 mice. The 10 μg/mL value is the scaffold loading concentration, not a systemic dose. [2]

Pyrintegrin did not show an apparent hepatocyte-engraftment benefit versus vehicle in a small mouse comparator experiment using 10 mg/kg intraperitoneally and imaging on days 3 and 5. These observations do not establish statistical equivalence or exclude effects under other conditions. [4]

Local scaffold-associated adipose tissue formation

Animal study · Male C57BL/6 mice; native inguinal fat-pad environment; N=6/group [2]

Pyrintegrin-loaded collagen/PCL scaffolds showed greater lipid-positive tissue formation and mouse PPARγ expression after 4 wk than pyrintegrin-free scaffolds. No cells were transplanted.

Measured endpoints — not treatment concentrations
EndpointReported resultReference
Scaffold lipid staining and mouse PPARγ expressionQualitative histology and qRT-PCR direction Greater Oil Red O-positive tissue and higher PPARγ in pyrintegrin-loaded scaffolds than control[2]

Conditions shared by the study groups

Route
Local implantation of collagen-infused PCL scaffold in the inguinal fat pad
Frequency
One implantation
Treatment course
4 wk
Vehicle
Type I collagen gel (3 mg/mL) in PCL scaffold
Study groups and reported outcomes
Group / doseComparatorObserved resultReference
Pyrintegrin-loaded scaffold
10 μg/mL pyrintegrin in collagen gel (loading concentration)		Pyrintegrin-free collagen gel in PCL scaffold; no cells transplanted in either groupMore Oil Red O-positive tissue and higher mouse PPARγ expression than pyrintegrin-free scaffolds[2]
Pyrintegrin-loaded scaffold
Model: Male C57BL/6 mice; inguinal fat-pad scaffold implantation; N=6/group
Reported limits: Loading concentration is not a systemic mg/kg dose or a measured tissue exposure. Release kinetics and drug exposure were not measured in the adopted experiment.
Methods and source locations

Compound reported in the paper: Pyrintegrin; Compound label in the paper: Ptn

Local scaffold experiment in a native adipose environment; not evidence for unrestricted adipogenesis at any site or systemic efficacy.

Figure 3A–C and caption; Results: Pyrintegrin promotes adipogenesis from host endogenous cells without cell transplantation; Methods: In vivo implantation of Pyrintegrin adsorbed scaffolds; Statistical analysis

Scaffold lipid staining and mouse PPARγ expression: 4-wk retrieval; N=6/group in Results; caption: means±SD, *P<0.05; methods: one-way ANOVA with Bonferroni tests. No numerical fold change inferred. — Figure 3B,C and caption; Results endogenous-cell subsection

Pyrintegrin-loaded scaffold · Figure 3A–C and caption; Results: Pyrintegrin promotes adipogenesis from host endogenous cells without cell transplantation; Methods: In vivo implantation of Pyrintegrin adsorbed scaffolds; Statistical analysis

Pyrintegrin comparator did not show hepatocyte engraftment enhancement

Animal study · Syngeneic hepatocyte transplantation in C57 mice, monitored by bioluminescence; n=3 in Figure 1 caption [4]

The pyrintegrin comparator did not show an apparent improvement over vehicle in day-3 or day-5 engraftment-associated imaging. The successful ripasudil comparator does not establish efficacy of pyrintegrin.

Measured endpoints — not treatment concentrations
EndpointReported resultReference
Bioluminescence after hepatocyte transplantationQualitative comparative imaging outcome No apparent increase for pyrintegrin versus vehicle at days 3 or 5[4]

Conditions shared by the study groups

Route
Intraperitoneal injection
Frequency
Administered soon after transplantation; repeat schedule for pyrintegrin not specified in the reviewed screening paragraph
Treatment course
Readouts on days 3 and 5
Vehicle
DMSO stock diluted 1:20 in 30% 2-hydroxypropyl-β-cyclodextrin
Study groups and reported outcomes
Group / doseComparatorObserved resultReference
Pyrintegrin comparator
10 mg/kg body weight		Matched working-solution vehicle controlNo apparent enhancement of engraftment-associated bioluminescence versus vehicle in the plotted day-3/day-5 data[4]
Pyrintegrin comparator
Model: Syngeneic luciferase-expressing hepatocyte transplantation into C57 mice; n=3 as caption states
Reported limits: Do not borrow the days 0,1,2 ripasudil regimen for pyrintegrin. Exact pyrintegrin versus vehicle p values are not supplied in the figure.
Methods and source locations

Compound reported in the paper: Pyrintegrin; Compound label in the paper: Pyrintegrin

Model-specific negative comparator with small n. Bioluminescence is an engraftment-associated surrogate and does not prove statistical equivalence.

Figure 1A–C and caption; initial Results paragraph; Methods: In vivo screening; Statistical analysis

Bioluminescence after hepatocyte transplantation: Means±SEM, n=3; no exact radiance values or p values inferred. Statistical methods describe unpaired two-tailed Student t tests. — Figure 1A–C and caption

Pyrintegrin comparator · Figure 1A–C and caption; initial Results paragraph; Methods: In vivo screening; Statistical analysis

Specifications

Manufacturer Adooq Bioscience
CAS Number 1228445-38-2
Formula C23H25N5O3S
Molecular Weight 451.54
SMILES
C1C(C1)CN[S](=O)(=O)C2=CC=C(C=C2)NC3=NC=CC(=N3)N4CCCC5=C4C=CC(=C5)O

Storage & Solubility

In Vitro Solubility

Reported Solubility

No reported solubility data are available for this product.

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. [1] Lee HW, Khan SQ, Faridi MH, et al. A Podocyte-Based Automated Screening Assay Identifies Protective Small Molecules. Journal of the American Society of Nephrology : JASN (2015). PMID: 25858967 DOI: 10.1681/asn.2014090859 Source material
  2. [2] Shah BS, Chen M, Suzuki T, et al. Pyrintegrin Induces Soft Tissue Formation by Transplanted or Endogenous Cells. Scientific reports (2017). PMID: 28128224 DOI: 10.1038/srep36402 Source material
  3. [3] Li Z, Fang J, Ge H, et al. Effect of fibrinogen like protein 1 on cisplatin-resistance in laryngeal carcinoma through targeting integrinβ1 in vivo and in vitro. Discover oncology (2025). PMID: 41171493 DOI: 10.1007/s12672-025-03337-x Source material
  4. [4] Ma H, Wang C, Liang S, et al. ROCK inhibition enhanced hepatocyte liver engraftment by retaining membrane CD59 and attenuating complement activation. Molecular therapy : the journal of the American Society of Gene Therapy (2023). PMID: 36860134 DOI: 10.1016/j.ymthe.2023.02.018 Source material

Publications

1 publication citing this product

  1. Zhen Li, .et al. , Discov Oncol, 2025, Oct 31;16(1):2000 PMID: 41171493

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