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Cat. No.: HY-183995

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SH-26

SH-26 is a PHD1 PROTAC degrader with DC₅₀s of 1.06 μM, 4.16 μM and 4.91 μM in MDA-MB-231, HepG2 and HEK-293T cells, respectively. SH-26 recruits CRBN to induce PHD1 degradation via the ubiquitin-proteasome system. SH-26 attenuates APAP (HY-66005)-triggered ROS accumulation, mitochondrial dysfunction, and NLRP3 inflammasome activation. SH-26 can be used for the research of acute liver injury.
(Pink: HIF/HIF Prolyl-Hydroxylase ligand (HY-183996); Blue: Cereblon ligand (HY-10984); Black: linker).

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

Formula: C₃₈H₄₁N₉O₈
Molecular Weight:751.79

Storage:

Please store the product under the recommended conditions in the Certificate of Analysis.

SH-26 Chemical Structure

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Fluorescent Dye

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

Biological Activity
- Description
- IC₅₀ & Target
- In Vitro
- Parmacokinetics
- In Vivo
Chemical Information
Purity & Documentation
References
Calculators
Help & FAQs
Bioz

Biological Activity

Description

SH-26 is a PHD1 PROTAC degrader with DC₅₀s of 1.06 μM, 4.16 μM and 4.91 μM in MDA-MB-231, HepG2 and HEK-293T cells, respectively. SH-26 recruits CRBN to induce PHD1 degradation via the ubiquitin-proteasome system. SH-26 attenuates APAP (HY-66005)-triggered ROS accumulation, mitochondrial dysfunction, and NLRP3 inflammasome activation. SH-26 can be used for the research of acute liver injury^[1]. (Pink: HIF/HIF Prolyl-Hydroxylase ligand (HY-183996); Blue: Cereblon ligand (HY-10984); Black: linker).

IC₅₀ & Target^[1]

NLRP3 inflammasome

PHD1

All PROTACs Isoforms :

All HIF/HIF Prolyl-Hydroxylase Isoforms :

All NOD-like Receptor (NLR) Isoforms :

In Vitro

SH-26 (Compound 26) (0.25-10 μM; 2-72 h) induces concentration- and time-dependent PHD1 degradation in MDA-MB-231 cells, with a DC₅₀ of 1.06 μM and a D_max of 77.5% in 48 h^[1].
SH-26 (0.25-50 μM; 48 h) induces concentration-dependent PHD1 degradation in HepG2 cells with a DC₅₀ of 4.16 μM^[1].
SH-26 (0-50 μM; 48 h) induces concentration-dependent PHD1 degradation in HEK-293T cells with a DC₅₀ of 4.91 μM^[1].
SH-26 (2-25 μM; 48 h) mediates PHD1 degradation in MDA-MB-231, HepG2, and HEK-293T cells in a ubiquitin-proteasome system-dependent manner that requires both PHD1 target engagement and CRBN recruitment^[1].
SH-26 (1-25 μM; 4 h pretreatment) degrades PHD1 and PHD2 (but not PHD3) and stabilizes HIF-1α in APAP-challenged AML12 hepatocytes under normoxic conditions^[1].
SH-26 (1-25 μM; 4 h pretreatment) exhibits enhanced concentration-dependent PHD1 degradation (DC₅₀ = 0.13 μM) and stabilizes HIF-1α in APAP-challenged AML12 hepatocytes under hypoxic conditions^[1].
SH-26 (1-50 μM; 4 h pretreatment) protects AML12 hepatocytes from APAP-induced injury in a concentration-dependent manner without inherent cytotoxicity^[1].
SH-26 (1-25 μM; 4 h pretreatment) restores expression of HIF-1α target genes BNIP3 and SLC2A1, does not affect PHD1 mRNA levels, and suppresses IL-1β mRNA levels in APAP-challenged AML12 hepatocytes^[1].
SH-26 (1-50 μM; 4 h pretreatment) dose-dependently degrades PHD1 and suppresses IL-1β protein levels in APAP-challenged AML12 hepatocytes^[1].
SH-26 (1 μM; 24 h) degrades PHD1 and downregulates pro-inflammatory mediators IL-1β, IL-6, and TNF-α in LPS (HY-D1056)+IFN-γ-stimulated THP-1-derived M1 macrophages^[1].
SH-26 (1-25 μM; 4 h pretreatment) dose-dependently reduces mitochondrial reactive oxygen species accumulation in APAP-challenged AML12 hepatocytes^[1].

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

Western Blot Analysis^[1]

Cell Line:

MDA-MB-231 breast cancer cells
Concentration:

0.25μM; 0.5 μM; 1 μM; 2 μM; 2.5 μM; 5 μM; 10 μM
Incubation Time:

2 h; 4 h; 8 h; 12 h; 24 h; 48 h; 72 h
Result:

Induced 67% PHD1 degradation at 24 h, 70% at 48 h, and 80% at 72 h at 2 μM.
Induced concentration-dependent PHD1 degradation with a DC₅₀ of 1.06 μM and a maximum degradation (D_max) of 77.5%.
Caused significant degradation within 4 h, with maximal depletion achieved by 72 h.
Showed no hook effect at concentrations up to 10 μM.

Western Blot Analysis^[1]

Cell Line:

HepG2 hepatoma cells
Concentration:

0.25μM; 0.5 μM; 1 μM; 2.5 μM; 5 μM; 10 μM
Incubation Time:

48 h
Result:

Induced concentration-dependent PHD1 degradation with a DC₅₀ of 4.16 μM.

Western Blot Analysis^[1]

Cell Line:

HEK-293T embryonic kidney cells
Concentration:

0.25μM; 0.5 μM; 1 μM; 2.5 μM; 5 μM; 10 μM
Incubation Time:

48 h
Result:

Induced concentration-dependent PHD1 degradation with a DC₅₀ of 4.91 μM.

Western Blot Analysis^[1]

Cell Line:

MDA-MB-231, HepG2, and HEK-293T cells
Concentration:

2 μM; 25 μM
Incubation Time:

48 h
Result:

Had its PHD1-degrading activity blocked in all three cell lines when cotreated with MG132, MLN4924, Takeda-54, or SH-28.

Western Blot Analysis^[1]

Cell Line:

AML12 hepatocytes
Concentration:

1 μM; 2.5 μM; 5 μM; 10 μM; 25 μM
Incubation Time:

4 h pretreatment
Result:

Degraded PHD1 in a concentration-dependent manner.
Degraded PHD2 with a DC₅₀ of 1.83 μM and a D_max of 71.8%.
Did not degrade PHD3.
Stabilized HIF-1α in a concentration-dependent manner.

Western Blot Analysis^[1]

Cell Line:

AML12 hepatocytes
Concentration:

1 μM; 2.5 μM; 5 μM; 10 μM; 25 μM
Incubation Time:

4 h pretreatment
Result:

Exhibited enhanced PHD1 degradation under hypoxia with a DC₅₀ of 0.13 μM.
Stabilized HIF-1α in a concentration-dependent manner.

Cell Viability Assay^[1]

Cell Line:

AML12 hepatocytes (APAP-induced injury)
Concentration:

1 μM; 2.5 μM; 5 μM; 10 μM; 25 μM; 50 μM
Incubation Time:

4 h pretreatment
Result:

Attenuated APAP-induced hepatotoxicity in a concentration-dependent manner.
Exhibited no inherent cytotoxicity at tested concentrations.

Real Time qPCR^[1]

Cell Line:

AML12 hepatocytes (APAP-induced injury)
Concentration:

1 μM; 5 μM; 25 μM
Incubation Time:

4 h pretreatment
Result:

Restored BNIP3 mRNA to baseline levels and significantly upregulated SLC2A1 mRNA at 10 μM.
Did not alter PHD1 mRNA levels.
Dose-dependently suppressed IL-1β mRNA levels.

Western Blot Analysis^[1]

Cell Line:

AML12 hepatocytes (APAP-induced injury)
Concentration:

1 μM; 2.5 μM; 5 μM; 10 μM; 25 μM; 50 μM
Incubation Time:

4 h pretreatment
Result:

Dose-dependently degraded PHD1.
Dose-dependently suppressed IL-1β protein levels.

Parmacokinetics

Species	Dose	Route	C_max	T_max	Plasma Concentration
Mice^[1]	30 mg/kg	i.p.	7 μM	0.5 h	~10 nM

In Vivo

SH-26 (Compound 26) (10-30 mg/kg; i.p.; single dose) confers robust hepatoprotective effects in APAP-induced acute liver injury^[1].

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

Animal Model:

C57BL/6 (male, 8 weeks old, APAP-induced acute liver injury)^[1]
Dosage:

10 mg/kg; 30 mg/kg
Administration:

i.p.; single dose
Result:

Significantly reduced serum levels of alanine aminotransferase (ALT), aspartate aminotransferase (AST), creatinine (CRE), and blood urea nitrogen (BUN) at 30 mg/kg.
Markedly attenuated APAP-induced hepatic damage, confirmed by histopathological analysis and necrotic area quantification at 10 mg/kg and 30 mg/kg.
Effectively reversed APAP-induced upregulation of PHD1 protein expression and induced robust PHD1 degradation in liver tissue at 10 mg/kg and 30 mg/kg.
Significantly reduced the upregulation of inflammasome components (NLRP3, GSDMD, cleaved caspase 1, cleaved IL-1β) at 10 mg/kg and 30 mg/kg.
Attenuated pro-apoptotic signals (increased BAX/BCL2 ratio, elevated cleaved caspase 3 levels) at 10 mg/kg and 30 mg/kg.
Significantly reduced liver tissue expression of immune cell markers LY6G, F4/80, CD31, and CD3 at 10 mg/kg and 30 mg/kg.

Chemical Information

Molecular Weight 751.79
Formula C₃₈H₄₁N₉O₈
SMILES

O=C1N(C(C2=CC=CC(NCCOCCOCCOCCNC(CCNC3=CC4=NC=NN4C(C5=C(C=C(C=C5)C#N)C)=C3)=O)=C21)=O)C6CCC(NC6=O)=O
Shipping

Room temperature in continental US; may vary elsewhere.
Storage

Please store the product under the recommended conditions in the Certificate of Analysis.

Purity & Documentation

Handling Instructions (2659 KB)

References

[1]. Su H, et al. Targeted Degradation of Prolyl Hydroxylase Domain Enzyme 1 (PHD1) as a Novel Therapeutic Strategy for Acetaminophen-Induced Acute Liver Injury. J Med Chem. 2026;69(10):12122-12143. [Content Brief]

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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.

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Biological Activity
- Description
- IC₅₀ & Target
- In Vitro
- In Vivo
Chemical Information
Purity & Documentation
References

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SH-26

All PROTACs Isoforms

All HIF/HIF Prolyl-Hydroxylase Isoforms

All NOD-like Receptor (NLR) Isoforms

Biological Activity

Chemical Information

Purity & Documentation

References

Calculators

Help & FAQs

SH-26 Related Classifications

Cat. No.: HY-183995