PROTAC ALK5 Degrader-1
PROTAC ALK5 Degrader-1 is a selective ALK5 PROTAC degrader. PROTAC ALK5 Degrader-1 induces ALK5 degradation via ALK5 ATP-binding pocket engagement, CRBN recruitment, and the ubiquitin-proteasome system.PROTAC ALK5 Degrader-1 inhibits ALK5 downstream signaling. PROTAC ALK5 Degrader-1 can be used for the research of pulmonary fibrosis.
(Pink: Anaplastic lymphoma kinase (ALK) ligand (HY-183441); Blue: Cereblon ligand (HY-14658); Black: linker (HY-183440)).
For research use only. We do not sell to patients.
- CAS No.: 3125240-35-6
- Formula: C43H43ClFN9O7
- Molecular Weight:852.31
-
Storage:
Please store the product under the recommended conditions in the Certificate of Analysis.
All PROTACs Isoforms
More
Biological Activity
PROTAC ALK5 Degrader-1 (Compound A31) (0.1-1 μM; 24 h) induces ALK5 degradation in NIH3T3 cells[1].
PROTAC ALK5 Degrader-1 (1 μM; 2-48 h) induces time-dependent ALK5 degradation in NIH3T3 cells[1].
PROTAC ALK5 Degrader-1 (0.37-30 μM; 24 h) induces concentration-dependent ALK5 degradation in NIH3T3 cells over 24 h[1].
PROTAC ALK5 Degrader-1 (1 μM; 48 h) selectively induces ALK5 degradation over the related ALK4 receptor in NIH3T3 cells[1].
PROTAC ALK5 Degrader-1 (1 μM; 48 h)-induced ALK5 degradation in NIH3T3 cells is reversible, with gradual recovery of ALK5 protein levels following compound wash-out after 48 h of 1 μM treatment[1].
PROTAC ALK5 Degrader-1 (1 μM; 48 h)-induced ALK5 degradation in NIH3T3 cells requires engagement of the ALK5 ATP-binding pocket, CRBN recruitment, and the ubiquitin-proteasome system[1].
PROTAC ALK5 Degrader-1 (1 μM; 48 h) suppresses phosphorylation of ALK5 downstream effectors Smad2/3, AKT, and ERK1/2 in TGF-β1-stimulated NIH3T3 cells[1].
PROTAC ALK5 Degrader-1 (0.2-5 μM; 48 h) dose-dependently inhibits TGF-β1-induced upregulation of fibrotic markers Collagen I and α-SMA in NIH3T3 cells[1].
PROTAC ALK5 Degrader-1 (0.2-5 μM; 48 h) dose-dependently reduces the fluorescence intensity of fibrotic markers Collagen I and α-SMA in TGF-β1-stimulated NIH3T3 cells following 1 h of TGF-β1 stimulation[1].
MedChemExpress (MCE) has not independently confirmed the accuracy of these methods. They are for reference only.
-
Cell Line:NIH3T3
-
Concentration:0.1 μM; 1 μM
-
Incubation Time:24 h
-
Result:Induced 18% ALK5 degradation at 0.1 μM.
Induced 49% ALK5 degradation at 1 μM.
-
Cell Line:NIH3T3
-
Concentration:1 μM
-
Incubation Time:2 h; 4 h; 8 h; 12 h; 24 h; 48 h
-
Result:Detected reduction in ALK5 levels starting at 24 h.
Showed progressive degradation over time, reaching maximal effect at 48 h.
-
Cell Line:NIH3T3
-
Concentration:0.37 μM; 1.1 μM; 3.3 μM; 10 μM; 30 μM
-
Incubation Time:24 h
-
Result:Elicited ALK5 degradation at 0.37 μM.
Showed most pronounced degradation effect at 1.1 μM.
Exhibited reduced degradation efficiency at concentrations above 1.1 μM, consistent with a hook effect-like phenomenon.
Did not achieve 50% degradation within the tested concentration range.
-
Cell Line:NIH3T3
-
Concentration:1 μM
-
Incubation Time:48 h
-
Result:Efficiently degraded ALK5.
Barely degraded ALK4 under the same experimental conditions.
Kept ALK5 protein levels suppressed under continuous treatment.
Showed gradual recovery of ALK5 protein levels after compound wash-out.
-
Cell Line:NIH3T3
-
Concentration:1 μM
-
Incubation Time:48 h
-
Result:Significantly reduced phosphorylation of Smad2/3, AKT, and ERK1/2.
Did not alter total protein levels of Smad2/3, AKT, and ERK1/2.
-
Cell Line:NIH3T3
-
Concentration:0.2 μM; 1 μM; 5 μM
-
Incubation Time:48 h
-
Result:Dose-dependently attenuated the TGF-β1-induced increase in Collagen I protein expression.
Dose-dependently attenuated the TGF-β1-induced increase in α-SMA protein expression.
-
Cell Line:NIH3T3
-
Concentration:0.2 μM; 1 μM; 5 μM
-
Incubation Time:48 h
-
Result:Dose-dependently reduced the fluorescence intensity of Collagen I.
Dose-dependently reduced the fluorescence intensity of α-SMA.
Confirmed attenuation of TGF-β1-induced fibroblast activation.
| Species | Dose | Route | AUC0-t | AUC0-∞ | MRT0-t | MRT0-∞ | T1/2 | Tmax | Cmax | F |
|---|---|---|---|---|---|---|---|---|---|---|
| Mice[1] | 1 mg/kg | i.v. | 264.94 μg/L·h | 263.61 μg/L·h | 0.48 h | 0.50 h | 1.33 h | 0.08 h | 678.84 μg/L | / |
| Mice[1] | 10 mg/kg | p.o. | 7.36 μg/L·h | 7.50 μg/L·h | 0.36 h | 0.48 h | 0.50 h | 0.08 h | 28.67 μg/L | 0.28 % |
| Mice[1] | 10 mg/kg | i.p. | 1869.79 μg/L·h | 1875.37 μg/L·h | 1.67 h | 1.75 h | 4.24 h | 0.33 h | 1139.89 μg/L | 70.57 % |
MedChemExpress (MCE) has not independently confirmed the accuracy of these methods. They are for reference only.
-
Animal Model:C57BL/6 (Bleomycin-induced pulmonary fibrosis model)[1]
-
Dosage:15 mg/kg; 30 mg/kg
-
Administration:i.p.; daily; 14 days
-
Result:Alleviated Bleomycin-induced body weight loss compared to vehicle-treated mice.
Reduced lung index by 10.6% at 15 mg/kg relative to dose-matched TP008.
Reduced fibrosis score by 9.8% at 15 mg/kg relative to dose-matched TP008, with efficacy comparable to nintedanib.
Reduced collagen positive percentage by 15.9% at 15 mg/kg relative to dose-matched TP008, restoring collagen levels toward sham control at both doses.
Reduced Collagen I fluorescence intensity by 15% and α-SMA fluorescence intensity by 20% at 15 mg/kg relative to dose-matched TP008, with efficacy comparable to nintedanib at both doses.
Reduced the proportion of lung dendritic cells (CD11c+ MHCII+) with greater efficacy than nintedanib, and attenuated bleomycin-induced accumulation of F4/80+ CD11b+ CD206+ macrophages with effects comparable to nintedanib, in a dose-dependent manner.
Reduced lung tissue ALK5 protein levels and suppressed downstream signaling activation (p-Smad2/3, p-AKT, p-ERK1/2) in a dose-dependent manner; showed greater suppression of p-AKT (additional 27%) and p-ERK1/2 (additional 79%) at 15 mg/kg relative to dose-matched TP008.
Showed no significant systemic toxicity: histopathology of heart, liver, spleen, and kidneys showed normal tissue architecture, and serum ALT/AST levels were not significantly different from sham controls.
Chemical Information
-
CAS No. 3125240-35-6
-
Molecular Weight 852.31
-
Formula C43H43ClFN9O7
-
SMILES
ClC1=CC(C2=CC(N3C4=CC=NC=C4N(CC(NCCN5CCN(CCCCOC6=CC=CC(C(N7C8C(NC(CC8)=O)=O)=O)=C6C7=O)CC5)=O)C3=O)=C(C)C=N2)=C(F)C=C1
-
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
References
Calculators
Concentration (start) × Volume (start) = Concentration (final) × Volume (final)