Fig. 1 · Structure

Cat. No.: A20680
CAS No.: 501364-82-5
Formula: C₂₃H₂₅N₃O₄S
Mol. Weight: 439.53

Documents & Downloads

INO-1001

Name: INO-1001
Brand: Adooq Bioscience
SKU: A20680
Availability: InStock
Rating: 5 (1 reviews)

Cat. No. A20680 CAS 501364-82-5

PARP inhibitor

INO-1001 is a potent and selective poly (ADP-ribose) polymerase (PARP) inhibitor.

In Stock

Free Aliquoting for Your Order

Tell us your preferred amount per vial. We’ll confirm the options.

Biological Activity

Bioactivity / Mechanism

INO-1001 showed approximately 30-fold preferential PARP1 versus PARP2 engagement in a duplexed cellular CeTEAM assay. This selectivity describes stabilization of mutant PARP biosensors in U-2 OS cells. The concurrent S/G2 shift (EC50 5.97e-008 M) is a trapping-like phenotype, rather than a direct measurement of PARP retention on DNA. [1]

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

Target & Activity

Target	Activity	Value
PARP

In Vitro Studies

In rd1 retinal explants, 0.1 µM INO1001 reduced PARP activity, PAR accumulation, calpain activity and TUNEL-positive photoreceptor cells relative to untreated rd1 cultures. General HDAC activity increased. Combining INO1001 with 5 µM JA2131 further lowered TUNEL positivity, without a further reduction in calpain activity. These ex-vivo findings do not establish an in-vivo retinal benefit. [2]

Retinal responses depended on the tested context. In Rho I255del/+ retinal explants, 10 µM INO1001 decreased PARP activity but increased TUNEL-positive photoreceptor cells; calpain activity was unchanged. This result limits broad neuroprotection claims across retinal disease models and concentrations. [3]

Cellular PARP1/PARP2 engagement and cell-cycle profiling

Cell-based study · Live human U-2 OS osteosarcoma cells expressing PARP1 L713F-GFP and PARP2 L269A-mCherry CeTEAM biosensors [1]

INO-1001 preferentially stabilized the PARP1 biosensor over PARP2 (approximately 30-fold). A concurrent S/G2 cell-cycle shift was reported, with EC50 5.97e-008 M. These are cellular biosensor/phenotype endpoints, not purified-enzyme IC50 values or direct PARP–DNA retention measurements.

Measured endpoints — not treatment concentrations
Endpoint	Reported result	Reference
Relative apparent cellular target engagement of PARP1 and PARP2 mutant biosensors	Approximate selectivity ~30-fold preference for PARP1	[1]
S/G2 shift from median Hoechst intensity (DNA content)	EC50 5.97e-008 M	[1]

Literature-Reported Treatment Conditions

Treatment concentration: Concentration gradient; EC50 values are assay endpoints, not a selected treatment dose.
Exposure duration: 24 h (Figure 3).
Method: Live-cell fluorescence microscopy with concurrent Hoechst DNA-content measurement.
Vehicle: 0.1% DMSO final for INO-1001; DMSO comparator.
Co-treatment: None for this profiling experiment.
Reported limits: Exact INO-1001 gradient bounds not transcribed from curves; no lot or salt designation in the read chemicals section.

Methods and source locations

Compound reported in the paper: INO-1001; Compound label in the paper: INO-1001

Evidence applies to the named study material and model. Salt form and analytical equivalence to the current catalog lot are not established; no salt conversion or lot-performance claim.

Figure 3A–F; Tables 1–2; Experimental procedures: Antibodies and chemicals, Live-cell fluorescence microscopy; Results: validation and selectivity sections

Relative apparent cellular target engagement of PARP1 and PARP2 mutant biosensors: Fluorescence accumulation normalized to DMSO; Figure 3B–D reports means from n = 3 experiments. — Results: Intracellular selectivity profiling; Figure 3B–D; Table 1, INO-1001 row

S/G2 shift from median Hoechst intensity (DNA content): Concurrent live-cell DNA-content analysis; Figure 3F overlay uses one representative experiment from n = 3. — Table 2, INO-1001 row; Figure 3E–F and caption

PARP inhibition in rd1 retinal explant treatment matrix

Cell-based study · Organotypic rd1 mouse retinal explants; wild-type explants provide baseline comparisons; cellular/ex-vivo intervention [2]

At 0.1 µM, INO1001 reduced PARP-activity-positive, PAR-positive, calpain-activity-positive and TUNEL-positive outer nuclear layer cells relative to untreated rd1 cultures. HDAC activity increased. Adding 5 µM JA2131 further reduced TUNEL positivity but did not further reduce calpain activity.

Measured endpoints — not treatment concentrations
Endpoint	Reported result	Reference
PARP-activity-positive cells in outer nuclear layer	Mean ± SD; % positive cells INO1001 2.60 ± 0.35 (n = 8); untreated rd1 3.75 ± 0.68 (n = 17); P < 0.01	[2]
PAR-positive cells in outer nuclear layer	Mean ± SD; % positive cells INO1001 1.22 ± 0.44 (n = 13); untreated rd1 1.94 ± 0.31 (n = 13); P < 0.001	[2]
Calpain-activity-positive cells in outer nuclear layer	Mean ± SD; % positive cells INO1001 2.63 ± 0.45 (n = 8); untreated rd1 3.93 ± 0.82 (n = 18); P < 0.01; combination 2.63 ± 0.45 (n = 8)	[2]
TUNEL-positive cells in outer nuclear layer	Mean ± SD; % positive cells Untreated rd1 4.91 ± 0.51 (n = 29); INO1001 3.47 ± 0.70 (n = 21); JA2131 3.48 ± 0.53 (n = 23); combination 2.49 ± 0.45 (n = 18); each treatment vs untreated rd1 P < 0.0001	[2]
HDAC-activity-positive cells in outer nuclear layer	Mean ± SD; % positive cells INO1001 3.70 ± 0.76 (n = 13); untreated rd1 2.34 ± 0.33 (n = 15); P < 0.0001	[2]

Literature-Reported Treatment Conditions

Treatment concentration: INO1001 0.1 µM; combination arm also contains JA2131 5 µM.
Exposure duration: Retinae explanted at P5 and assessed at P11; medium changed with treatment every 2 days.
Method: Exposure in organotypic retinal explant medium.
Vehicle: Compounds dissolved in DMSO; final medium ≤0.1% DMSO. Reported comparator is untreated rd1, with untreated wild type as baseline.
Co-treatment: INO1001 monotherapy and INO1001 + JA2131 combination distinguished; JA2131-only and 8-Br-ADPR arms provide pathway comparisons.
Reported limits: A separate start time after explantation and a matched vehicle-only group are not explicitly specified in the read culture-method paragraph. No analytical lot validation.

Methods and source locations

Compound reported in the paper: INO-1001; Compound label in the paper: INO1001

Evidence applies to the named study material and model. Salt form and analytical equivalence to the current catalog lot are not established; no salt conversion or lot-performance claim.

Figures 2–4 and captions; embedded Additional Tables 2–3; Methods: Organotypic retinal explant culture, marker assays, Microscopy and image analysis; relevant Results/Discussion

PARP-activity-positive cells in outer nuclear layer: In situ fluorescent NAD+ incorporation assay; one-way ANOVA/Tukey comparisons. — Figure 2B–C; Additional Table 2, PARP activity rows

PAR-positive cells in outer nuclear layer: PAR immunostaining; one-way ANOVA/Tukey comparisons. — Figure 2D–E; Additional Table 2, PAR rows

Calpain-activity-positive cells in outer nuclear layer: In situ calpain activity assay; one-way ANOVA/Tukey comparisons; combination did not add to monotherapy effect. — Figure 3A–B; Additional Table 2, calpain activity rows; associated Results

TUNEL-positive cells in outer nuclear layer: TUNEL staining; one-way ANOVA/Tukey; counts are labeled samples n in the table, not inferred numbers of animals. — Figure 4C–D; Additional Table 3, TUNEL rows

HDAC-activity-positive cells in outer nuclear layer: General in situ HDAC assay; assay does not identify which HDAC/sirtuin isoform contributes. — Figure 4A–B; Additional Table 3, HDAC activity rows

Dose-dependent effects in a dominant rhodopsin-mutant retinal explant model

Cell-based study · Organotypic Rho I255del/+ mouse retinal explants; untreated mutant control and wild-type comparison [3]

At 10 µM, INO1001 reduced PARP-activity-positive cells but increased TUNEL-positive photoreceptor cells. Calpain activity did not change significantly. The 0.1 and 1 µM groups did not show the significant effects highlighted for 10 µM; the rd1 protective finding must not be generalized across retinal models.

Measured endpoints — not treatment concentrations
Endpoint	Reported result	Reference
Outer nuclear layer PARP-activity-positive cells	Direction and reported significance Reduced at 10 µM; ** p ≤ 0.01	[3]
Outer nuclear layer photoreceptor cell death	Direction and reported significance Increased TUNEL positivity at 10 µM; ** p ≤ 0.01	[3]
Outer nuclear layer calpain activity	Reported null result No significant change with INO1001 in this dose series	[3]

Literature-Reported Treatment Conditions

Treatment concentration: 0.1, 1 and 10 µM INO1001.
Exposure duration: Explant culture P12–P20; drug treatment from P14 to P20, medium changed every second day.
Method: Exposure in organotypic retinal explant medium.
Vehicle: DMSO in culture medium; non-treated (NT) comparator. Separate DMSO control groups (0.01%, 0.1%, 1%) are described in Methods.
Co-treatment: INO1001 single agent; other PARP inhibitors tested in parallel, not combined.
Reported limits: Exact final DMSO concentration for each INO1001 dose not specified in the read treatment paragraph. Tables S7/S9 not retrieved as usable supplement; no exact group mean or per-group n inferred from dots.

Methods and source locations

Compound reported in the paper: INO-1001; Compound label in the paper: INO1001

Evidence applies to the named study material and model. Salt form and analytical equivalence to the current catalog lot are not established; no salt conversion or lot-performance claim.

Table 1; Methods 2.2 and 2.9; Results 3.5; Figure 5A–F and caption

Outer nuclear layer PARP-activity-positive cells: In situ activity assay; Figure 5 caption gives 3–14 independent retinal cultures across panels, SD error bars and two-way ANOVA/Dunnett comparisons. — Results 3.5; Figure 5A–B and caption

Outer nuclear layer photoreceptor cell death: TUNEL assay; no exact percentage estimated from plotted points. — Results 3.5; Figure 5E–F and caption

Outer nuclear layer calpain activity: In situ calpain assay; absence of significance is not proof of equivalence. — Results 3.5; Figure 5C–D and caption

In Vivo Studies

In male Apoe-deficient mice on a Western-type diet, daily intraperitoneal INO-1001 at 1 mg/kg for 10 weeks reduced aortic-root fractional and maximum stenosis versus 5% glucose vehicle (15 mice per group). Plasma lipids were not significantly changed, and the authors did not establish increased plaque stability in this model. [4]

Atherosclerotic lesion development in Apoe-deficient mice

Animal study · Male Apoe−/− mice fed a Western-type diet, 15 per group [4]

INO-1001 treatment was associated with reduced aortic-root fractional and maximum stenosis compared with glucose vehicle. Lipid concentrations were not significantly changed, and increased plaque stability was not established in this model.

Measured endpoints — not treatment concentrations
Endpoint	Reported result	Reference
Aortic-root atherosclerotic stenosis	Direction; Mann–Whitney U comparisons Fractional stenosis reduced, P = 0.001; maximum stenosis reduced, P = 0.01; n = 15/group	[4]
Plasma triglycerides, total cholesterol, LDL cholesterol and HDL cholesterol	Reported null results No significant between-group differences (Table 2: n.s.; n = 15/group)	[4]
Plaque stability-related collagen content and vascular smooth-muscle cell amount	Limiting result No increase in collagen content or amount of VSMCs established	[4]

Conditions shared by the study groups

Route: Intraperitoneal
Frequency: Daily
Treatment course: 10 weeks
Vehicle: 5% glucose

Study groups and reported outcomes
Group / dose	Comparator	Observed result	Reference
INO-1001 versus glucose vehicle 1 mg/kg body weight/day	5% glucose vehicle; n = 15 per group.	Aortic-root fractional stenosis reduced (P = 0.001) and maximum stenosis reduced (P = 0.01). No increase in plaque stability was established; Table 2 reports no significant plasma-lipid differences.	[4]

INO-1001 versus glucose vehicle: Model: Male Apoe−/− mice, B6.129P2 strain; 8 weeks old at entry; Western-type diet.; Reported limits: Named Inotek material; salt and lot unspecified. Do not reconstruct precise mean/median ± summaries because reporting conventions conflict.

Methods and source locations

Compound reported in the paper: INO-1001; Compound label in the paper: INO-1001

Evidence applies to the named study material and model. Salt form and analytical equivalence to the current catalog lot are not established; no salt conversion or lot-performance claim.

Methods: Animals, Tissue Processing and Statistical Analysis; Results: plaque effects; Figure 2; Table 2; Discussion

Aortic-root atherosclerotic stenosis: Oil Red O-stained serial aortic-root sections and morphometric analysis; box-plot conventions from Figure 2 caption. — Figure 2A–D and caption; Results: Effects of INO-1001 Treatment on Atherosclerotic Plaques; Methods: Tissue Processing and Statistical Analysis

Plasma triglycerides, total cholesterol, LDL cholesterol and HDL cholesterol: Blood analysis at tissue harvesting, age 18 weeks. No equivalence or lipid-lowering effect claimed. — Table 2; Results: Animal/Blood Analysis

Plaque stability-related collagen content and vascular smooth-muscle cell amount: Discussion assessment; underlying numerical data not shown in the read main article, so no effect size extracted. — Discussion: paragraph beginning “Beside lesion progression”

INO-1001 versus glucose vehicle · Methods: Animals, Tissue Processing, Statistical Analysis; Results: Animal/Blood Analysis and Effects of INO-1001 Treatment on Atherosclerotic Plaques; Figure 2; Table 2; Discussion

Specifications

Manufacturer	Adooq Bioscience
Actions	Inhibitor
CAS Number	501364-82-5
Applications	PARP inhibitor
Formula	C₂₃H₂₅N₃O₄S
Molecular Weight	439.53
Synonyms	IN01001
SMILES	O=C1NC2=C(CC3=C2C=CC(S(NCCCN4CCOCC4)(=O)=O)=C3)C5=CC=CC=C51

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] Pires MJ, Alam S, Lovric A, et al. Duplexed CeTEAM drug biosensors reveal determinants of PARP inhibitor selectivity in cells. The Journal of biological chemistry (2025). PMID: 40021124 DOI: 10.1016/j.jbc.2025.108361 Source material
[2] Yan J, Kong L, Zhao Z, et al. Poly(ADP-ribose) polymerase regulates transient receptor potential channel M2-dependent calpain activation in rd1 mouse retinal degeneration. Neural regeneration research (2026). PMID: 41641786 DOI: 10.4103/nrr.nrr-d-24-01102 Source material
[3] Zhu Y, Fallatah AHA, Jiao K, et al. PARP Activity Is Essential for Retinal Photoreceptor Survival in the Human Homologous RhoI255del Mouse Model for Autosomal Dominant Retinitis Pigmentosa. Journal of neurochemistry (2025). PMID: 41427648 DOI: 10.1111/jnc.70319 Source material
[4] Erbel C, Achenbach J, Akhavanpoor M, et al. PARP inhibition in atherosclerosis and its effects on dendritic cells, T cells and auto-antibody levels. European journal of medical research (2011). PMID: 21813379 DOI: 10.1186/2047-783x-16-8-367 Source material

Publications

1 publication citing this product

Jie Yan, .et al. , Neural Regen Res, 2026, Oct 1;21(10):5044-5051 PMID: 41641786

You May Also Consider

A10019 CAS 934162-61-5

A-966492

A-966492 displayed high potency against the poly(ADP-ribose) polymerase-1 (PARP-1) enzyme with a K(i) of 1 nM and an EC(50) of 1 nM in a whole cell assay.

Starting at $20.00

View Sizes