2. Autophagy PROTAC Metabolic Enzyme/Protease
  3. AUTACs HIF/HIF Prolyl-Hydroxylase
  4. HATC

HATC is a HIF-1α AUTAC degrader. HATC links HIF-1α to LC3 to form a ternary complex that undergoes degradation via the autophagy-lysosome fusion pathway. HATC induces dose-dependent HIF-1α degradation in multiple cell types. HATC reduces visceral fat accumulation, hepatic lipid deposition, senescent cell aggregation, and bone loss; alleviates age-related intervertebral disc degeneration, liver dysfunction, kyphosis, and alveolar dilation; decreases circulating lactic acid levels; improves physical performance; and reverses age-related changes in granulocyte proportions. HATC extends median and maximum lifespan, reduces transcriptomic age, and causes no obvious persistent toxicity. HATC can be used in the research of age-related diseases (pink: LC3 ligand (HY-50759); blue: HIF-1α ligand (HY-P10426); Linker: (HY-W008264)).

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HATC

HATC 構造式

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HATC 関連抗体

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HIF-1α HIF

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製品説明

HATC is a HIF-1α AUTAC degrader. HATC links HIF-1α to LC3 to form a ternary complex that undergoes degradation via the autophagy-lysosome fusion pathway. HATC induces dose-dependent HIF-1α degradation in multiple cell types. HATC reduces visceral fat accumulation, hepatic lipid deposition, senescent cell aggregation, and bone loss; alleviates age-related intervertebral disc degeneration, liver dysfunction, kyphosis, and alveolar dilation; decreases circulating lactic acid levels; improves physical performance; and reverses age-related changes in granulocyte proportions. HATC extends median and maximum lifespan, reduces transcriptomic age, and causes no obvious persistent toxicity. HATC can be used in the research of age-related diseases (pink: LC3 ligand (HY-50759); blue: HIF-1α ligand (HY-P10426); Linker: (HY-W008264))[1].

IC50 & Target[1]

HIF-1α

 

体外実験

HATC (1-2 μM) potently induces autophagic degradation of HIF-1α in NP cells at 5% oxygen with no cytotoxicity at concentrations up to 2 μM[1].
HATC induces autophagic degradation of HIF-1α in 293T and HeLa cells under hypoxic conditions[1].

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

HATC 関連抗体
Parmacokinetics
Species Dose Route Plasma Concentration
Mice[1] 20 mg/kg i.p. 0.3 μM
体内実験

HATC (20 mg/kg; i.p.; once weekly) extends median lifespan by 14% and maximum lifespan by 12.1% in aged C57BL/6J mice, while improving healthspan across multiple physiological and pathological aging metrics[1].
HATC (20 mg/kg; i.p.; once weekly) reduces HIF-1α levels and alleviates lumbar spine instability-induced accelerated intervertebral disc aging in mice[1].

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

Animal Model: C57BL/6J mice (male and female, aged 20 months at treatment initiation)[1]
Dosage: 20 mg/kg
Administration: i.p.; once weekly; until natural death
Result: Extended median lifespan by 14% and maximum lifespan by 12.1% compared to vehicle.
Mitigated age-associated weight gain and prevented rapid terminal weight loss, maintaining stable body weight until late life.
Reduced HIF-1α levels across multiple organs (lung, spleen, liver) compared to vehicle-treated aged mice.
Lowered predicted transcriptomic age in 24-month-old mice, with transcriptomic changes showing upregulation of pathways linked to improved organ function and metabolic health.
Reduced abdominal visceral fat accumulation and hepatic lipid deposition, prevented age-related increases in serum alanine aminotransferase and aspartate aminotransferase levels, and lowered circulating lactate levels to near young-mouse levels.
Improved multiple physical performance metrics (grip strength, maximal walking speed, bean balance time, hanging endurance, daily activity) to values approaching young mice.
Reduced age-related bone mass loss in female mice, improved spinal kyphosis index (lower spinal curvature), and attenuated age-dependent alveolar volume expansion in the lungs.
Reduced P16INK4a-positive senescent cells in organs, decreased inflammatory cell invasion in lung and liver, lowered circulating levels of SASP markers (IL-6, G-CSF), and reversed age-related increases in granulocyte proportion.
Reduced spontaneous tumor incidence by ~20% compared to vehicle-treated mice.
Animal Model: mice (aged 9 months at treatment initiation, LSI-induced aging model)[1]
Dosage: 20 mg/kg
Administration: i.p.; once weekly; 3 months
Result: Significantly reduced HIF-1α levels in IVDs within 2 weeks of treatment initiation.
Alleviated age-related disc degeneration, as shown by improved histological scores on Safranin O/Fast Green staining, higher T2-weighted MRI signal intensity in IVDs, increased paw withdrawal threshold (reduced low back pain), and reduced P16INK4a-positive senescent cell accumulation in IVDs compared to vehicle-treated LSI mice.
Caused no overt toxicity or tissue damage in major organs (lung, spleen, liver) as assessed by H&E staining.
分子量

1477.19

分子式

C79H102ClN13O13
SMILES

O=C1N(CC2=CC=CC=C2)C([C@@H](C(C)C)N(CCCNC(CCOCCOCCOCCN3C=C(C[C@H](NC([C@H](CC4=CC=C(O)C=C4)N5)=O)C(N[C@@H](CC(C)C)C(N[C@@H](CC(C)C)C(N[C@@H](CC6=CC=CC=C6)C(N[C@@H](C(C)C)C5=O)=O)=O)=O)=O)N=N3)=O)C(C7=CC=C(C)C=C7)=O)=NC8=CC(Cl)=CC=C18
輸送条件

Room temperature in continental US; may vary elsewhere.
保管条件

Please store the product under the recommended conditions in the Certificate of Analysis.
純度とドキュメンテーション
参考文献
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HATC Related Classifications

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

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

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濃度 （開始） × 体積 （開始） = 濃度 （終了） × 体積 （終了）
× = ×
C1   V1   C2   V2
Help & FAQs
  • Do most proteins show cross-species activity?

    Species cross-reactivity must be investigated individually for each product. Many human cytokines will produce a nice response in mouse cell lines, and many mouse proteins will show activity on human cells. Other proteins may have a lower specific activity when used in the opposite species.

Keywords:

HATCAUTACsHIF/HIF Prolyl-HydroxylaseAutophagy-targeting chimerasHypoxia-inducible factorsHIFsHIF-PHautophagy-lysosome fusionHIF-1α293T cellsSASP markersC57BL/6J miceNP cellsHeLa cellsintervertebral disc agingLC3senescent cellInhibitorinhibitorinhibit

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