Cat. No.: HY-13817

IU1

25 Cited Publications

Customer Review

Based on 25 publication(s) in Google Scholar

IU1 is a selective, reversible USP14 inhibitor with an IC₅₀ of 4-5 μM. IU1 binds USP14’s catalytic cleft to block deubiquitinase activity. IU1 induces calpain-dependent Tau cleavage, causes ATP deficits, reduces E1~Ub thioester levels and 26S proteasome assembly. IU1 enhances 26S proteasome chymotrypsin-like activity, modulates LC3B-dependent autophagy flux, reduces cancer cell proliferation and migration, and blocks G0/G1 to S phase cell cycle transition in follicular thyroid cancer cells. IU1 activates autophagy-lysosomal and ubiquitin-proteasome pathways, triggers apoptosis, and reduces cervical cancer cell growth. IU1 enhances degradation of proteasome substrates linked to neurodegenerative disease, accelerates oxidized protein degradation, and increases oxidative stress resistance. IU1 can be used for the research of Alzheimer’s disease, follicular thyroid cancer, ischemic stroke, cervical cancer, and neurodegenerative disease.

For research use only. We do not sell to patients.

Purity: 99.30%
CAS No.: 314245-33-5
Formula: C₁₈H₂₁FN₂O
Molecular Weight:300.37

Storage:

Powder -20°C, 3 years , 4°C, 2 years ; In solvent -80°C, 6 months , -20°C, 1 month

IU1 Chemical Structure

CAS No.: 314245-33-5

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Fluorescent Dye

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

Biological Activity
- Description
- IC₅₀ & Target
- In Vitro
- In Vivo
Chemical Information
Publications (25)
Solvent & Solubility
- In Vitro
- In Vivo
Purity & Documentation
References
Help & FAQs
Bioz

Biological Activity

Description

IC₅₀ & Target^[1]

USP14

4-5 μM (IC₅₀)

All Deubiquitinase Isoforms :

In Vitro

IU1 (75 μM; 6-22 h) reduces Prostaglandin J2 (PGJ2) (HY-113366)-induced ubiquitinated protein accumulation, induces calpain-dependent cleavage of Tau, α-spectrin, and pro-caspase 3, and does not alter basal ubiquitinated protein levels in rat embryonic (E18) cerebral cortical neuronal cultures^[1].
IU1 (5-50 μM; 4-24 h) is neurotoxic in a concentration-dependent and time-dependent manner, with 5 μM IU1 causing significant viability loss after 24 h, and 25 μM IU1 inducing toxicity as early as 4 h^[1].
IU1 (5-80 μM; 4-24 h) reduces intracellular ATP levels in a concentration-dependent manner (significant at ≥25 μM after 24 h) and time-dependent manner (significant at 25 μM after 24 h)^[1].
IU1 directly inhibits mitochondrial Complex I activity with an IC₅₀ of ~40 μM for NADH:Q1 reductase activity, has minimal effects on Complex II, and increases Complex IV activity at high concentrations, without altering ATP synthase function in permeabilized rat brain mitochondrial membranes^[1].
IU1 (5-50 μM; 16 h) abolishes basal E1-Ub thioester levels, reduces PGJ2-induced ubiquitinated protein accumulation, and significantly reduces total E1 protein levels when co-treated with PGJ2; IU1 concentrations ≤25 μM have minimal effects on E1-Ub thioester, E1 protein, and ubiquitinated protein levels in rat embryonic (E18) cerebral cortical neuronal cultures^[1].
IU1 (5-50 μM; 24 h) induces a concentration-dependent decline in 26S proteasome assembly and activity, with a concomitant increase in 20S proteasome activity and levels, with 50 μM IU1 causing the most pronounced effects in rat embryonic (E18) cerebral cortical neuronal cultures^[1].
IU1 (1-100 μM; 24 h) dose-dependently reduces the viability of ML1 follicular thyroid cancer cells, with significant effects observed at 30, 50, and 100 μM, while having minimal impact on primary human thyroid cell viability^[2].
IU1 (20 μM; 6 h) significantly reduces basal migration of both ML1 follicular thyroid cancer cells and primary human thyroid cells, and abolishes S1P-stimulated migration in ML1 cells^[2].
IU1 (20-50 μM; 24 h) increases the chymotrypsin-like activity of 26S proteasomes in ML1 follicular thyroid cancer cells, with 20 μM inducing a stronger significant effect^[2].
IU1 (50 μM; 24 h) significantly inhibits the catalytic activity of USP14 in ML1 follicular thyroid cancer cells, while 20 μM IU1 has no significant effect on USP14 catalytic activity^[2].
IU1 (20 μM; 24 h) enhances LC3B-dependent autophagy flux in ML1 follicular thyroid cancer cells while reducing LC3B-dependent autophagy flux in primary human thyroid cells when co-treated with 100 μM CQ for 4 h^[2].
IU1 (20 μM; 24 h) does not alter SQSTM1/p62 protein expression in ML1 follicular thyroid cancer cells or primary human thyroid cells, either alone or in combination with 100 μM CQ^[2].
IU1 (20 μM; 6 h) significantly reduces basal migration of FTC-133 follicular thyroid cancer cells^[2].
IU1 (25 μM; 4 h reoxygenation after 8 h OGD) increases ZO-1 protein expression in OGD-treated cultured Bend.3 brain endothelial cells, preventing OGD-induced ZO-1 reduction^[3].
IU1 (0.1-100 μM; 24 h; 100 μM; 12, 24, 48 h) suppresses the proliferation of HeLa and SiHa human cervical cancer cells in a dose- and time-dependent manner^[4].
IU1 (2, 50, 100 μM for HeLa; 20, 50, 100 μM for SiHa; 1 week) reduces long-term colony formation of HeLa and SiHa human cervical cancer cells after 1 week of culture^[4].
IU1 (100 μM; 24, 48 h) impairs 2D migration of HeLa and SiHa human cervical cancer cells, as measured by reduced wound closure at 24 and 48 h^[4].
IU1 (2, 50, 100 μM for HeLa; 20, 50, 100 μM for SiHa; 12 h) induces G0/G1 cell cycle arrest and reduces S/G2/M phase populations after 12 h of treatment^[4].
IU1 (2-100 μM; 12 h) induces dose-dependent apoptosis in HeLa human cervical cancer cells after 12 h of treatment^[4].
IU1 (100 μM; 12 h) reduces MDM2 protein expression and increases p53 protein expression in HeLa human cervical cancer cells after 12 h of treatment; IU1 (2-100 μM; 12 h) increases levels of cleaved caspase-3, cleaved caspase-9, and cleaved caspase-8 to promote apoptosis^[4].
IU1 (0.1-100 μM; 12 h) enhances UPS function in HeLa human cervical cancer cells by increasing total protein ubiquitination in a dose-dependent manner after 12 h of treatment^[4].
IU1 (0.1-2 μM; 12 h) increases p62 and LC3-II protein levels, while IU1 (5-100 μM; 12 h) decreases p62 and increases LC3-II protein levels, in HeLa human cervical cancer cells after 12 h of treatment, indicating autophagy activation^[4].
IU1 (100 μM; 12 h post 48 h transfection) increases LC3 puncta formation and the number of autophagosomes and autolysosomes in HeLa human cervical cancer cells transfected with pBabe-EGFP-mRFP-LC3, confirming autophagy activation^[4].
IU1 (4.7-100 μM; ~30 min-2 hr) potently and selectively inhibits the deubiquitinating activity of proteasome-bound human Usp14, with an IC₅₀ of 4.7 μM, and this inhibition is fully reversible^[5].
IU1 (34 μM; 0, 4, 8 min) enhances proteasomal degradation of polyubiquitinated cyclin B in vitro by inhibiting Usp14^[5].
IU1 (25-100 μM; 6 hr) reduces Tau protein levels in wild-type MEFs by enhancing proteasomal degradation via Usp14 inhibition^[5].
IU1 (10-100 μM; 6 hr) reduces protein levels of both expanded (Q80) and wild-type (Q22) ataxin-3 in wild-type MEFs by enhancing proteasomal degradation via Usp14 inhibition^[5].
IU1 (75 μM; 0, 2, 4, 6, 8 hr) reduces TDP-43 protein levels and enhances its ubiquitination in wild-type MEFs by enhancing proteasomal degradation via Usp14 inhibition^[5].
IU1 (50 μM; 6 hr) does not affect the levels of the ubiquitin-independent proteasome substrate cODC-EGFP in wild-type MEFs, demonstrating its effect is specific to ubiquitin-dependent proteasomal substrates via Usp14 inhibition^[5].

MedChemExpress (MCE) has not independently confirmed the accuracy of these methods. They are for reference only.

Cell Proliferation Assay^[2]

Cell Line:

ML1 follicular thyroid cancer cells, primary human thyroid cells
Concentration:

1 μM, 3 μM, 5 μM, 10 μM, 20 μM, 30 μM, 50 μM, and 100 μM
Incubation Time:

24 h
Result:

Significantly reduced ML1 cell proliferation at 100 μM.
Caused dose-dependent reductions in ML1 cell proliferation at 20, 30, 50, and 100 μM, with 100 μM inducing the strongest effect.
Significantly reduced primary thyroid cell proliferation only at 100 μM.

Western Blot Analysis^[2]

Cell Line:

ML1 follicular thyroid cancer cells
Concentration:

20-50 μM
Incubation Time:

24 h
Result:

Decreased the total amount of mature 26S proteasome complexes at 20 and 50 μM, with 50 μM inducing a significant reduction.
Reduced the amount of USP14-containing 26S proteasome complexes, though this decrease did not reach statistical significance.

Western Blot Analysis^[2]

Cell Line:

ML1 follicular thyroid cancer cells, primary human thyroid cells
Concentration:

20 μM (IU1); 100 μM (Chloroquine
, co-treatment)
Incubation Time:

24 h (IU1); 4 h (CQ, final incubation)
Result:

Significantly increased LC3B-II levels in ML1 cells when co-treated with 100 μM Chloroquine, indicating enhanced LC3B-dependent autophagy flux.
Significantly reduced LC3B-II levels in primary thyroid cells when co-treated with 100 μM Chloroquine, indicating reduced LC3B-dependent autophagy flux.\nDid not cause significant changes in GABARAP-II levels in either ML1 cells or primary thyroid cells when co-treated with 100 μM Chloroquine, indicating no effect on GABARAP-dependent autophagy flux.

Cell Proliferation Assay^[4]

Cell Line:

HeLa, SiHa human cervical cancer cells
Concentration:

0.1-100 μM (24 h); 100 μM (12, 24, 48 h)
Incubation Time:

12 h, 24 h, 48 h (100 μM); 24 h (0.1-100 μM)
Result:

Significantly decreased cell proliferation in a dose-dependent and time-dependent manner in both HeLa and SiHa cells.

Cell Migration Assay^[4]

Cell Line:

HeLa, SiHa human cervical cancer cells
Concentration:

100 μM
Incubation Time:

24 h, 48 h
Result:

Markedly suppressed wound closure in both HeLa and SiHa cells at 24 and 48 h compared to controls.

Cell Cycle Analysis^[4]

Cell Line:

HeLa, SiHa human cervical cancer cells
Concentration:

2, 50, 100 μM (HeLa); 20, 50, 100 μM (SiHa)
Incubation Time:

12 h
Result:

Dramatically induced G0/G1 cell cycle arrest, associated with a decreased population in S/G2/M phases.

Apoptosis Analysis^[4]

Cell Line:

HeLa human cervical cancer cells
Concentration:

2, 50, 100 μM
Incubation Time:

12 h
Result:

Significantly increased the relative apoptosis ratio in HeLa cells, with dose-dependent increases in early (Q4), late (Q2), and total apoptotic cells.

Western Blot Analysis^[4]

Cell Line:

HeLa human cervical cancer cells
Concentration:

100 μM (MDM2/p53 analysis); 2, 20, 50, 100 μM (caspase analysis)
Incubation Time:

12 h
Result:

Decreased MDM2 protein expression and increased p53 protein expression at 100 μM compared to controls.
Increased protein levels of cleaved caspase-3, cleaved caspase-9, and cleaved caspase-8 at 2, 20, 50, and 100 μM.

Western Blot Analysis^[4]

Cell Line:

HeLa human cervical cancer cells
Concentration:

0.1-2 μM; 5-100 μM
Incubation Time:

12 h
Result:

Increased p62 and LC3-II protein levels in a dose-dependent manner at 0.1-2 μM.
Decreased p62 protein levels and increased LC3-II protein levels in a dose-dependent manner at 5-100 μM.

Immunofluorescence^[4]

Cell Line:

HeLa human cervical cancer cells (transfected with pBabe-EGFP-mRFP-LC3)
Concentration:

100 μM
Incubation Time:

12 h (after 48 h vector transfection)
Result:

Significantly increased the number of EGFP and mRFP LC3 puncta per cell, as well as the number of autophagosomes and autolysosomes per cell.

In Vivo

IU1 (400 μg/kg; intraperitoneally; immediately after reperfusion, then 24 hours and 48 hours post-ischemic stroke) protects blood-brain barrier integrity, attenuates neuroinflammation, reduces infarct volume by ~40%, and improves motor function recovery in MCAO mice^[3].

MedChemExpress (MCE) has not independently confirmed the accuracy of these methods. They are for reference only.

Animal Model:

ICR mice (male, adult, 8-10 weeks old, 25-28 g, middle cerebral artery occlusion surgery with 60 minutes of occlusion followed by reperfusion)^[3]
Dosage:

400 μg/kg
Administration:

intraperitoneally; immediately after reperfusion, then 24 hours and 48 hours post-ischemic stroke
Result:

Reduced USP14 protein expression in brain tissue and reduced USP14-positive vascular cells per field.
Increased Zonula occludens 1 (ZO-1) protein expression in brain tissue.
Reduced myeloperoxidase (MPO) protein expression in brain tissue compared to MCAO controls and reduced MPO-positive leukocytes in ischemic brain tissue.
Reduced ionized calcium-binding adapter molecule 1 (IBA1)-positive microglial cells per field compared to MCAO controls.
Reduced glial fibrillary acidic protein (GFAP) protein expression in brain tissue compared to MCAO controls and reduced activated GFAP-positive astrocytes.
Reduced brain tissue levels of proinflammatory cytokines TNF-α, IL-1β, and IL-6 compared to MCAO controls.
Reduced infarct volume compared to MCAO controls.
Increased NeuN-positive neuron count per field compared to MCAO controls and reduced TUNEL-positive apoptotic neurons per field compared to MCAO controls.

Chemical Information

CAS No. 314245-33-5
Appearance Solid
Molecular Weight 300.37
Formula C₁₈H₂₁FN₂O
Color Light yellow to yellow
SMILES

CC1=CC(C(CN2CCCC2)=O)=C(C)N1C3=CC=C(F)C=C3
Shipping

Room temperature in continental US; may vary elsewhere.

Storage

Powder	-20°C	3 years
	4°C	2 years
In solvent	-80°C	6 months
	-20°C	1 month

Publications (25)

All Cell Proliferation/Viability AssayWBCell Migration/Invasion AssayIn Vivo Efficacy StudyHistological Imaging/Staining

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Journal Impact Factor

Cancer Cell

Ubiquitination-directed cytosolic DNA degradation governs cGAS-STING-mediated immune response to DNA damage. [Abstract]

2026 Feb 9;44(2):306-320.e7. PMID: 41512867
Nat Commun

USP2 inhibition unleashes CD47-restrained phagocytosis and enhances anti-tumor immunity. [Abstract]

2025 May 16;16(1):4564. PMID: 40379682
Nat Commun

USP8 inhibition reshapes an inflamed tumor microenvironment that potentiates the immunotherapy. [Abstract]

2022 Mar 31;13(1):1700. PMID: 35361799
Cell Death Differ

A self-amplifying USP14-TAZ loop drives the progression and liver metastasis of pancreatic ductal adenocarcinoma. [Abstract]

2023 Jan;30(1):1-15. PMID: 35906484

IU1 purchased from MedChemExpress. Usage Cited in: Cell Death Differ. 2023 Jan;30(1):1-15. [Abstract]

PANC-1 and SW1990 cells were stained with CFSE and plated into 6-well plates for 12 h of incubation. After 48 h IU1 treatment, flow cytometry was used to examine the cell proliferation.

IU1 purchased from MedChemExpress. Usage Cited in: Cell Death Differ. 2023 Jan;30(1):1-15. [Abstract]

Transwell assay was used to measure the migration and invasion of the PANC-1 and SW-1990 cells treated with IU1.

IU1 purchased from MedChemExpress. Usage Cited in: Cell Death Differ. 2023 Jan;30(1):1-15. [Abstract]

Tumour volumes were measured with the vehicle-treated group and the IU1 (40 mg/kg, i.g.)-treated group.

IU1 purchased from MedChemExpress. Usage Cited in: Cell Death Differ. 2023 Jan;30(1):1-15. [Abstract]

H&E staining and IHC staining of Ki67 and TAZ from the corn oil-treated group and the IU1 (40 mg/kg, i.g.)-treated group.
Adv Sci (Weinh)

USP35 Acts as a Deubiquitinating Enzyme for ID3 to Promote Immune Escape in Colorectal Cancer. [Abstract]

2026 Jan 4:e16588. PMID: 41486422

IU1 purchased from MedChemExpress. Usage Cited in: Adv Sci (Weinh). 2026 Jan 4:e16588. [Abstract]

Western blot analysis of ID3 and PD‐L1 levels under different IU1 (0.31, 0.62, 1.25, 2.50, 5.00 μM, or 1.25 μM, 2, 6, 9, 12, 18, 24 h) concentrations.
Sci Adv

The cohesin-associated protein Pds5A governs the meiotic spindle assembly via deubiquitination of Kif5B in oocytes. [Abstract]

2025 Apr 11;11(15):eadt6159. PMID: 40215310
Redox Biol

USP20 governs tyrosine kinase inhibitors resistance through ferroptosis evasion by targeting GPX4 in cancers. [Abstract]

2026 May:92:104086. PMID: 41844497
J Immunother Cancer

CD47 destabilization via manipulating the SPOP-USP2 axis augments macrophage phagocytosis and cancer immunotherapy. [Abstract]

2026 Jan 14;14(1):e013498. PMID: 41534899
Pharmacol Res

Nuclear receptor coactivator 4-mediated ferritinophagy contributes to cerebral ischemia-induced ferroptosis in ischemic stroke. [Abstract]

2021 Dec:174:105933. PMID: 34634471
Cell Death Dis

The deubiquitination enzyme USP14 promotes the tumourigenesis of gastric cancer by enhancing c-MYC nuclear translocation through deubiquitination of KPNA2. [Abstract]

2025 Oct 21;16(1):737. PMID: 41120255
Int J Biol Macromol

Mechanistic insights into the role of USP14 in adipose tissue macrophage recruitment and insulin resistance in obesity. [Abstract]

2024 Apr 15;267(Pt 2):131645. PMID: 38631582
EMBO J

USP8 promotes cancer progression and extracellular vesicle-mediated CD8+ T cell exhaustion by deubiquitinating the TGF-β receptor TβRII. [Abstract]

2022 Aug 16;41(16):e108791. PMID: 35811497
J Transl Med

USP14 inhibition promotes DNA damage repair and represses ovarian granulosa cell senescence in premature ovarian insufficiency. [Abstract]

2024 Sep 11;22(1):834. PMID: 39261935
Respir Res

The MFGE8/integrin β3 axis mitigates experimental neutrophilic asthma by suppressing NLRP3-Caspase-1 pathway-mediated NETosis. [Abstract]

2025 Jul 2;26(1):229. PMID: 40605028
iScience

Targeting USP14 enhances immunotherapy response by reprogramming tumor-associated macrophages in colon cancer. [Abstract]

2026 Mar 13;29(5):115362. PMID: 42058892
Sci Rep

Ubiquitin-specific protease 14 inhibition promotes mitophagy and attenuates neural apoptosis after spinal cord injury. [Abstract]

2025 Dec 9;15(1):43741. PMID: 41366047
Neurotoxicology

Inhibition of P2X7R by hypericin improves diabetic cardiac autonomic neuropathy through the proteasome- Nrf2 - GPX4 signaling axis. [Abstract]

2025 Jul:109:1-10. PMID: 40412558
Microbiol Spectr

miR-30a enhanced RIG-I-mediated type I interferon antiviral response by targeting USP14. [Abstract]

2025 Aug 5;13(8):e0018825. PMID: 40662581
Food Chem Toxicol

Piceatannol upregulates USP14-mediated GPX4 deubiquitination to inhibit neuronal ferroptosis caused by cerebral ischemia-reperfusion in mice. [Abstract]

2025 Jan 27:115281. PMID: 39880152
Front Oncol

Huaier Extract Inhibits Prostate Cancer Growth via Targeting AR/AR-V7 Pathway. [Abstract]

2021 Feb 23;11:615568. PMID: 33708629
Anim Cells Syst

2023 Nov 27.
Clin Transl Oncol

USP14 targets FABP5-mediated ferroptosis to promote proliferation and cisplatin resistance of HNSCC. [Abstract]

2025 Aug;27(8):3485-3500. PMID: 39928282
Eur J Histochem

Deubiquitinase USP14 is upregulated in Crohn's disease and inhibits the NOD2 pathway mediated inflammatory response in vitro. [Abstract]

2024 Sep 9;68(3):4101. PMID: 39252535
J Biosciences

46, 19 (2021).
Res Sq

2025 May 06.

Solvent & Solubility

In Vitro:

DMSO : 41.67 mg/mL (138.73 mM; Need ultrasonic; Hygroscopic DMSO has a significant impact on the solubility of product, please use newly opened DMSO)

View the Complete Stock Solution Preparation Table

Preparing Stock Solutions

View the Complete Stock Solution Preparation Table

Concentration Solvent Mass

1 mg

5 mg

10 mg

Concentration

Solvent

Mass

1 mM

3.3292 mL

16.6461 mL

33.2923 mL

5 mM

0.6658 mL

3.3292 mL

6.6585 mL

10 mM

0.3329 mL

1.6646 mL

3.3292 mL

Please refer to the solubility information to select the appropriate solvent. Once prepared, please aliquot and store the solution to prevent product inactivation from repeated freeze-thaw cycles.

Storage method and period of stock solution: -80°C, 6 months; -20°C, 1 month. When stored at -80°C, please use it within 6 months. When stored at -20°C, please use it within 1 month.

Molarity Calculator

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

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Dilution Calculator

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

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In Vivo:

Select the appropriate dissolution method based on your experimental animal and administration route.

Stock Solution Working Solution

For the following dissolution methods, please ensure to first prepare a clear stock solution using an In Vitro approach and then sequentially add co-solvents:
To ensure reliable experimental results, the clarified stock solution can be appropriately stored based on storage conditions. As for the working solution for In Vivo experiments, it is recommended to prepare freshly and use it on the same day.
The percentages shown for the solvents indicate their volumetric ratio in the final prepared solution. If precipitation or phase separation occurs during preparation, heat and/or sonication can be used to aid dissolution.

Protocol 1

Add each solvent one by one: 10% DMSO 40% PEG300 5% Tween-80 45% Saline

Solubility: ≥ 1.67 mg/mL (5.56 mM); Clear solution

This protocol yields a clear solution of ≥ 1.67 mg/mL (saturation unknown).

Taking 1 mL working solution as an example, add 100 μL DMSO stock solution (16.7 mg/mL) to 400 μL PEG300, and mix evenly; then add 50 μL Tween-80 and mix evenly; then add 450 μL Saline to adjust the volume to 1 mL.

Protocol 2

Add each solvent one by one: 10% DMSO 90% (20% SBE-β-CD in Saline)

Solubility: ≥ 1.67 mg/mL (5.56 mM); Clear solution

This protocol yields a clear solution of ≥ 1.67 mg/mL (saturation unknown).

Taking 1 mL working solution as an example, add 100 μL DMSO stock solution (16.7 mg/mL) to 900 μL 20% SBE-β-CD in Saline, and mix evenly.

Protocol 3

Add each solvent one by one: 10% DMSO 90% Corn Oil

Solubility: ≥ 1.67 mg/mL (5.56 mM); Clear solution

This protocol yields a clear solution of ≥ 1.67 mg/mL (saturation unknown). If the continuous dosing period exceeds half a month, please choose this protocol carefully.

Taking 1 mL working solution as an example, add 100 μL DMSO stock solution (16.7 mg/mL) to 900 μL Corn oil, and mix evenly.

In Vivo Dissolution Calculator

Please enter the basic information of animal experiments:

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g
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Recommended: Prepare an additional quantity of animals to account for potential losses during experiments.

Recommended: Prepare an additional quantity of animals to account for potential losses during experiments.

Please enter your animal formula composition:

%
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Recommended: Keep the proportion of DMSO in working solution below 2% if your animal is weak.
%
+
+
%
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%
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The co-solvents required include: DMSO, . All of co-solvents are available by MedChemExpress (MCE). , Tween 80. All of co-solvents are available by MedChemExpress (MCE).

Working solution concentration: 0.22 mg/mL

Purity & Documentation

Select Batch:

Purity: 99.98%

Assay: 99.98%

ee.: 99.98%

Data Sheet (295 KB)
SDS (476 KB)
- English - EN (476 KB)
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- Deutsch - DE (476 KB)
- Norwegian - NO (476 KB)
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COA (2659 KB)
Elemental Analysis Report (2659 KB)
HNMR (2659 KB)
CNMR (2659 KB)
RP-HPLC (2659 KB)
NP-HPLC (2659 KB)
MS (2659 KB)
LCMS (2659 KB)
IR (2659 KB)
GC (2659 KB)
OR (2659 KB)
SDS-PAGE (2659 KB)
SEC-HPLC (2659 KB)
Other Report (2659 KB)
Handling Instructions (2659 KB)

References

[1]. Kiprowska MJ, et al. Neurotoxic mechanisms by which the USP14 inhibitor IU1 depletes ubiquitinated proteins and Tau in rat cerebral cortical neurons: Relevance to Alzheimer's disease. Biochim Biophys Acta Mol Basis Dis. 2017;1863(6):1157-1170. [Content Brief]

[2]. Srinivasan V, et al. Proliferation and migration of ML1 follicular thyroid cancer cells are inhibited by IU1 targeting USP14: role of proteasome and autophagy flux. Front Cell Dev Biol. 2023;11:1234204. Published 2023 Aug 30. [Content Brief]

[3]. Hou W, et al. USP14 inhibition promotes recovery by protecting BBB integrity and attenuating neuroinflammation in MCAO mice. CNS Neurosci Ther. 2023;29(11):3612-3623. [Content Brief]

[4]. Xu L, et al. IU1 suppresses proliferation of cervical cancer cells through MDM2 degradation. Int J Biol Sci. 2020;16(15):2951-2963. Published 2020 Sep 16. [Content Brief]

[5]. Lee BH, et al. Enhancement of proteasome activity by a small-molecule inhibitor of USP14. Nature. 2010;467(7312):179-184. [Content Brief]

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.

Complete Stock Solution Preparation Table

Storage method and period of stock solution: -80°C, 6 months; -20°C, 1 month. When stored at -80°C, please use it within 6 months. When stored at -20°C, please use it within 1 month.

Optional Solvent	Concentration Solvent Mass	1 mg	5 mg	10 mg	25 mg
DMSO	1 mM	3.3292 mL	16.6461 mL	33.2923 mL	83.2307 mL
	5 mM	0.6658 mL	3.3292 mL	6.6585 mL	16.6461 mL
	10 mM	0.3329 mL	1.6646 mL	3.3292 mL	8.3231 mL
	15 mM	0.2219 mL	1.1097 mL	2.2195 mL	5.5487 mL
	20 mM	0.1665 mL	0.8323 mL	1.6646 mL	4.1615 mL
	25 mM	0.1332 mL	0.6658 mL	1.3317 mL	3.3292 mL
	30 mM	0.1110 mL	0.5549 mL	1.1097 mL	2.7744 mL
	40 mM	0.0832 mL	0.4162 mL	0.8323 mL	2.0808 mL
	50 mM	0.0666 mL	0.3329 mL	0.6658 mL	1.6646 mL
	60 mM	0.0555 mL	0.2774 mL	0.5549 mL	1.3872 mL
	80 mM	0.0416 mL	0.2081 mL	0.4162 mL	1.0404 mL
	100 mM	0.0333 mL	0.1665 mL	0.3329 mL	0.8323 mL

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IU1

Apoptosis Compound Library

Cell Cycle/DNA Damage Compound Library

Anti-Cancer Compound Library

Autophagy Compound Library

Peptidomimetic Library

Anti-Aging Compound Library

Anti-Cardiovascular Disease Compound Library

Endocrinology Compound Library

Ubiquitination Compound Library

Anti-Parkinson's Disease Compound Library

Neurodegenerative Disease-related Compound Library

Targeted Diversity Library

Metabolic Enzyme Compound Library

Protease Inhibitor Library

Highly Selective Inhibitors Library

Highly Selective Activators Library

Cell Death Library

Anti-Drug-Resistant Compound Library

Mitophagy Compound Library

Bioactive Compound Library Max

Bioactive Compound Library

Non-Alcoholic Fatty Liver Disease (NAFLD) Compound Library

High-Throughput Bioactive Compound Library

Posttranslational Modification Library

Publications Citing Use of MedChemExpress (MCE) IU1

All Deubiquitinase Isoforms

Biological Activity

Chemical Information

Publications (25)

Solvent & Solubility

Purity & Documentation

References

Help & FAQs

Complete Stock Solution Preparation Table

IU1

Apoptosis Compound Library

Cell Cycle/DNA Damage Compound Library

Anti-Cancer Compound Library

Autophagy Compound Library

Peptidomimetic Library

Anti-Aging Compound Library

Anti-Cardiovascular Disease Compound Library

Endocrinology Compound Library

Ubiquitination Compound Library

Anti-Parkinson's Disease Compound Library

Neurodegenerative Disease-related Compound Library

Targeted Diversity Library

Metabolic Enzyme Compound Library

Protease Inhibitor Library

Highly Selective Inhibitors Library

Highly Selective Activators Library

Cell Death Library

Anti-Drug-Resistant Compound Library

Mitophagy Compound Library

Bioactive Compound Library Max

Bioactive Compound Library

Non-Alcoholic Fatty Liver Disease (NAFLD) Compound Library

High-Throughput Bioactive Compound Library

Posttranslational Modification Library

Publications Citing Use of MedChemExpress (MCE) IU1

All Deubiquitinase Isoforms

Biological Activity

Chemical Information

Publications (25)

Solvent & Solubility

Purity & Documentation

References

Help & FAQs

Complete Stock Solution Preparation Table

IU1 Related Classifications

Cat. No.: HY-13817