Autophagy is a conserved cellular degradation and recycling process in the lysosome.There are three main types of autophagy in mammalian cells: macroautophagy, chaperone-mediated autophagy (CMA), and microautophagy. While CMA uses chaperones to identify cargo proteins and then unfolds and transfers them into the lysosome, macroautophagy sequesters cargo by autophagosomes—de novo synthesized of double-membrane vesicles—and then transports it to the lysosome. Microphagy captures cargoes by means of invaginations or protrusions of the lysosomal membrane directly.
The most well-studied form of autophagy, macroautophagy, is low-level and occurs by default. However, under stress conditions, such as nutrient or energy deprivation, it can also be further induced. The ubiquitin-proteasome system (UPS), a crucial protein degradation pathway, collaborates with stress-induced macrophagy to play a significant role in protein catabolism.
As the research went on, it was discovered that autophagy plays a crucial role in the catabolism of a variety of cellular components, including protein aggregates (aggrephagy), lipid droplets (lipophagy), iron complexes (Ferritinophagy), and carbohydrates. Except for macromolecules, autophagy can also target several organelles and structures, such as mitochondria (mitophagy), peroxisome (pexophagy), endoplasmic reticulum (reticulophagy or ER-phagy), ribosome (ribophagy), spermatozoon-inherited organelles following fertilization (allophagy), secretory granules within pancreatic cells (zymophagy) and intracellular pathogens (xenophagy).
Numerous human pathologies, such as aging, cancer, neurodegenerative disease, heart disease, and metabolic diseases like diabetes, are linked to autophagy and its dysfunction. Numerous prescription medications and herbal remedies affect autophagy through various signaling pathways. Small molecules that control autophagy appear to have a great deal of promise for treating these diseases in animal models or in clinical settings.
| Structure | Cat No. | Product Name | CAS No. | Product Description |
|---|---|---|---|---|
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V55037 | (3R,5S)-Fluvastatin ((3R,5S)-XU 62-320 free acid) | 155229-75-7 | (3R,5S)-Fluvastatin is the 3R,5S-isomer of Fluvastatin. |
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V55026 | (3R,5S)-Fluvastatin sodium ((3R,5S)-XU 62-320) | 94061-80-0 | (3R,5S)-Fluvastatin ((3R,5S)-XU 62-320) sodium is the 3R,5S-isomer of Fluvastatin. |
|
V55034 | (3S,5R)-Fluvastatin-d6 ((3S,5R)-XU 62-320-d6 free acid) | 2249799-34-4 | (3S,5R)-Fluvastatin-d6 is the deuterated form of (3S,5R)-Fluvastatin sodium. |
|
V56484 | (R)-(-)-Felodipine-d5 | 1217744-87-0 | (R)-(-)-Felodipine-d5 is the deuterated form of (R)-(-)-Felodipine. |
|
V51844 | (R,R)-LRRK2-IN-7 | 2307277-92-3 | (R,R)-LRRK2-IN-7 is an isomer of LRRK2-IN-7 . |
|
V56518 | (rac)-(trans)-Paroxetine-d4 hydrochloride | 1217753-24-6 | (rac)-(trans)-Paroxetine-d4 (HCl) is the deuterium labelled form of (rac)-(trans)-Paroxetine HCl. |
|
V52972 | (Rac)-BL-918 | 2435589-07-2 | (Rac)-BL-918 is the racemate of BL-918. |
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V52758 | (Rac)-Efavirenz-d4 | 1246812-58-7 | (Rac)-Efavirenz-d4 is the deuterated racemate of Efavirenz. |
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V55043 | (Rac)-MTK458 ((Rac)-EP-0035985) | 2499962-44-4 | EP-0035985 (Compound 16) is an activator of mitophagy. |
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V36067 | (Rac)-Sitagliptin ((Rac)-MK-0431) | 823817-56-7 | (Rac)-Sitagliptin is an isomer of Sitagliptin. |
|
V56464 | (rel)-ML-SI3 (trans-ML-SI3) | 2108567-79-7 | (rel)-ML-SI3 is an isomer of ML-SI3 . |
|
V55039 | (S)-Sitagliptin phosphate ((S)-MK-0431 phosphate) | 823817-58-9 | (S)-Sitagliptin phosphate is the less active S-isomer of Sitagliptin phosphate. |
|
V55038 | (±)-Taxifolin ((±)-Dihydroquercetin; (±)-Dihydroquercetin) | 24198-97-8 | (±)-Taxifolin ((±)-Dihydroquercetin) is the racemate of Taxifolin. |
|
V52507 | 3,4-Dimethoxychalcone | 5416-71-7 | 3,4-Dimethoxychalcone is a potential antibacterial and antioxidant. |
|
V56467 | 4-Hydroxytolbutamide-d9 (Hydroxytolbutamide-d9) | 1185112-19-9 | 4-Hydroxytolbutamide-d9 is the deuterated form of 4-Hydroxytolbutamide. |
|
V5167 | Aminolevulinic acid HCl (ALA) | 5451-09-2 | 5-Aminolevulinic acid HCl (also known as ALA hydrochloride; trade name: Levulan), an FDA approved drug for treating actinic keratosis, is an intermediate in heme biosynthesis and the universal precursor of tetrapyrroles. |
|
V56503 | AGN 193109-d7 | 1216429-25-2 | AGN 193109-d7 is the deuterium labelled form of AGN 193109. |
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V52434 | AGN 194310 (VTP-194310) | 229961-45-9 | AGN 194310 (VTP-194310) is a high-affinity, potent, and selective pan-antagonist of retinoic acid receptors (RARs) with Kds of 3 nM and 2 nM for RARα, RARβ, and RARγ respectively. |
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V55040 | AGN 205327 | 2070018-29-8 | AGN 205327 is a RAR agonist/activator with EC50s of 3766/734/32 nM for RARα/β/γ respectively, and has no inhibitory effect on RXR. |
|
V2090 | Aloe-emodin (Rhabarberone) | 481-72-1 | Aloe emodin (also known as NSC 38628, Rhabarberone; 3-Hydroxymethylchrysazine) is a hydroxyanthraquinone based and naturally occuring CFTR channel activator found in Aloe vera leaves, andhas a specific in vitro and in vivo antitumor activity. |
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