DU145 cell growth is inhibited by astaxanthin (50, 100, 150, and 200 µM; 48 hours) (IC50<200 µM) [1]. By preventing proliferation, promoting apoptosis, and hindering migration and invasion, astaxanthin (200 µM; 24 hours) lowers the expression of STAT3 and related pathway proteins (at the protein and mRNA levels) [1]. Additionally, astaxanthin shields RPE cells from oxidative stress and abnormal activation brought on by high glucose by downregulating VEGF at the protein level [2]. In K562 cells, astaxanthin (1-50 µM; 72 hours) increases the expression of the PPARγ protein in a dose- and time-dependent way [3].

DU145 cell growth is inhibited by astaxanthin (50, 100, 150, and 200 µM; 48 hours) (IC50<200 µM) [1]. By preventing proliferation, promoting apoptosis, and hindering migration and invasion, astaxanthin (200 µM; 24 hours) lowers the expression of STAT3 and related pathway proteins (at the protein and mRNA levels) [1]. Additionally, astaxanthin shields RPE cells from oxidative stress and abnormal activation brought on by high glucose by downregulating VEGF at the protein level [2]. In K562 cells, astaxanthin (1-50 µM; 72 hours) increases the expression of the PPARγ protein in a dose- and time-dependent way [3].

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Astaxanthin significantly suppressed the proliferation of human prostate cancer DU145 cells in a dose-dependent manner, as measured by MTT assay after 48 hours of treatment. Inhibition rates were 27%, 38%, and 50% at concentrations of 50 µM, 100 µM, and 200 µM, respectively, compared to the control. The half-inhibitory concentration (IC50) was reported to be less than 200 µM. [1]
Western blot analysis showed that treatment of DU145 cells with 200 µM Astaxanthin for 24 hours reduced the protein expression level of STAT3. [1]
RT-PCR analysis confirmed that 200 µM Astaxanthin treatment for 24 hours downregulated the mRNA expression level of STAT3. [1]
A colony formation assay demonstrated that 200 µM Astaxanthin treatment for 24 hours inhibited the cloning ability of DU145 cells, with a colony inhibition rate of 48%. When combined with siRNA-mediated STAT3 knockdown (si-STAT3), the inhibition rate was enhanced to 83%. [1]
Flow cytometry analysis using Annexin V-FITC/PI staining showed that treating DU145 cells with 200 µM Astaxanthin for 24 hours increased the percentage of apoptotic cells from 8.5% (control) to 13.1%. The combination of Astaxanthin and si-STAT3 further increased apoptosis to 18.5%. [1]
Transwell migration and invasion assays revealed that 200 µM Astaxanthin treatment for 24 hours decreased the migration and invasion abilities of DU145 cells. The migration inhibition rate was about 41%, and the invasion inhibition rate was about 36% compared to the control. The combination with si-STAT3 enhanced these inhibition rates to 71% and 56%, respectively. [1]
Western blot and RT-PCR analyses further indicated that Astaxanthin treatment downregulated the expression of STAT3 pathway-related proteins and genes (JAK2, Bcl-2, NF-κB p65) and upregulated pro-apoptotic proteins and genes (Bax, Caspase-3, Caspase-9). [1]

In mice that are not clothed, astaxanthin (200 mg/kg; gavaged once daily for three weeks) prevents the formation of tumor xenografts (DU145) [1]. In rats, astaxanthin (125 or 500 mg/kg; in animal feed; 7 days) significantly lowers oxidative stress and offers cardioprotection [4].

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In a DU145 xenograft tumor model established in nude mice, intragastric administration of Astaxanthin at a dose of 200 mg/kg once daily for 3 weeks significantly suppressed tumor growth compared to the control group receiving saline. [1]
The tumor growth suppressive effect of Astaxanthin was enhanced when combined with intratumoral delivery of si-STAT3. [1]

Apoptosis analysis [1]
Cell Types: DU145 Cell
Tested Concentrations: 200 µM (pre-incubation)
Incubation Duration: 24 hrs (hours)
Experimental Results: The percentage of apoptotic cells increased from 8.5% to 13.1% (compared to blank control).

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Cell migration assay[1]
Cell Types: DU145 Cell
Tested Concentrations: 200 µM
Incubation Duration: 24 hrs (hours)
Experimental Results: DU145 cells demonstrated diminished migration and invasion (approximately 41% of cells could not move from one chamber to another, 36% of cells could did not pass through the Transwell membrane compared to the control group).

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Cell proliferation assay[2]
Cell Types: ARPE-19 Cell
Tested Concentrations: 50 µM (pre-incubation)
Incubation Duration: 7 days
Experimental Results: Cell proliferation was Dramatically diminished when exposed to high glucose.

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Western Blot Analysis[1]
Cell Types: DU145 Cell
Tested Concentrations: 200 µM
Incubation Duration: 24 h
Experimental Results: The expression of STAT3 was diminished at both the protein and mRNA levels (down-regulated the protein expression of JAK2, BCL-2 and NF-κB, up-regulated BAX , protein express

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MTT Assay for Cell Viability/Proliferation: DU145 cells were seeded into 96-well plates at a density of 10^3-10^4 cells per well. Cells were treated with various concentrations of Astaxanthin (0, 50, 100, 200 µM) for 48 hours. Subsequently, MTT solution was added to each well and incubated for 4 hours. The formed formazan crystals were dissolved with DMSO, and the absorbance was measured at 490 nm using a plate reader. [1]
Colony Formation Assay: DU145 cells were treated according to experimental groups (e.g., transfected with si-STAT3 or control siRNA for 48 hours, followed by 200 µM Astaxanthin treatment for 24 hours). After treatment, a limited number of cells were seeded and cultured for 10-14 days to allow colony formation. The colonies were then fixed with 4% paraformaldehyde, stained with 0.1% crystal violet, and counted. [1]
Apoptosis Assay by Flow Cytometry: DU145 cells from different treatment groups were collected, stained with Annexin V-FITC and propidium iodide (PI) in the dark for 5 minutes, and then analyzed by flow cytometry to determine the percentage of apoptotic cells. [1]
Cell Migration and Invasion Assay (Transwell): For migration assays, treated DU145 cells were resuspended in medium containing 2% serum and seeded into the upper chamber of a Transwell insert. The lower chamber was filled with medium containing 10% serum as a chemoattractant. After 16 hours of incubation, cells that migrated to the lower side of the membrane were fixed with 4% paraformaldehyde, stained with crystal violet, and counted under a microscope. For invasion assays, the upper chamber membrane was pre-coated with Matrigel before seeding the cells; otherwise, the procedure was identical to the migration assay. [1]
Western Blot Analysis: DU145 cells treated under various conditions were lysed to extract total protein. Equal amounts of protein (30 µg) were separated by SDS-PAGE, transferred to a membrane, and probed with specific primary antibodies against STAT3, JAK2, Bcl-2, Bax, Caspase-3, Caspase-9, NF-κB p65, and β-actin (as a loading control). Protein bands were visualized using an appropriate detection system. [1]
RT-PCR (Reverse Transcription Polymerase Chain Reaction): Total RNA was extracted from treated DU145 cells using a commercial lysis reagent. One microgram of RNA was reverse-transcribed into cDNA. Quantitative PCR was performed using specific primers for STAT3, JAK2, Bcl-2, Bax, Caspase-3, Caspase-9, NF-κB p65, and β-actin to assess mRNA expression levels. [1]

Animal/Disease Models: Nude mouse (approximately 20 grams; DU145 tumor xenograft model) [1].
Doses: 200 mg/kg
Route of Administration: intragastric (po) (po)administration; one time/day for 3 weeks.
Experimental Results: It has a significant inhibitory effect on tumor growth.

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Animal/Disease Models: Female C57BL/6 mice (7 weeks old) [4].
Doses: 125 or 500 mg/kg
Route of Administration: Animal feed; 7 days.
Experimental Results: The mean infarct size was Dramatically diminished to 45.1% and 39.1% in the two treatment groups (125 and 500 mg/kg), respectively. The myocardial salvage rates in the 125 mg/kg group and 500 mg/kg group were 26% and 36%, respectively. 9-HETE levels were Dramatically diminished in a dose-dependent manner. 9-HETE is a regioisomer oxidation product of arachidonic acid and is thought to be a product of free radical-mediated oxidation.

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DU145 Xenograft Tumor Model in Nude Mice: DU145 cells in the logarithmic growth phase were subcutaneously inoculated into the left armpit of nude mice (2 x 10^7 cells per mouse). After tumors formed (approximately 2 weeks), tumor-bearing mice were randomly divided into groups. One group received intragastric administration of Astaxanthin at a dose of 200 mg/kg body weight once daily. The drug was prepared as a suspension with a concentration of 40 mg/mL, and 100 µL of this suspension was administered per mouse (assuming an average mouse weight of 20 g). The control group received an equivalent volume of saline. The treatment continued for 3 weeks, after which the mice were sacrificed, tumors were excised and weighed. Another experimental arm involved inoculating mice with DU145 cells that had been pre-transfected with si-STAT3 or control vector 24 hours prior to inoculation, followed by Astaxanthin or vehicle treatment as described. [1]

Absorption, Distribution and Excretion
This study compared the apparent digestibility coefficient (ADC) and carotenoid composition of astaxanthin (3,3'-dihydroxy-β,β-carotene-4,4'-dione) in muscle, liver, whole kidney, and plasma of Atlantic salmon (Salmo salar) and Atlantic halibut (Hippoglossus hippoglossus) after 112 days of feeding with a diet supplemented with 66 mg/kg dry matter astaxanthin. The astaxanthin source consisted of 75% all-trans-astaxanthin, 3% 9Z-astaxanthin, and 22% 13Z-astaxanthin, with (3R,3'R)-astaxanthin, (3R,3'S; meso)-astaxanthin, and (3S,3'S)-astaxanthin in a ratio of 1:2:1. After 56 and 112 days of feeding, the apparent digestibility (ADC) of astaxanthin in Atlantic halibut was significantly higher than that in Atlantic salmon (P < 0.05). The apparent digestibility of all-trans astaxanthin was significantly higher than that of 9Z-astaxanthin (P < 0.05). The carotenoid content in all plasma and tissue samples of salmon was significantly higher than that of halibut. The retention rate of astaxanthin in salmon muscle was 3.9%, while that in halibut was 0%. Compared with diet, all-trans astaxanthin selectively accumulated in salmon muscle and in the plasma of both salmon and halibut. Compared with plasma, 13Z-astaxanthin selectively accumulated in the liver and whole kidney of both salmon and halibut. The 3',4'-cis and trans glycolic acid isomers of iodoflavin (3,3',4'-trihydroxy-β,β-carotene-4'-one) were detected in halibut plasma, liver, and whole kidney, indicating that its astaxanthin metabolic pathway is similar to that of salmon. In summary, the apparent digestibility (ADC) of astaxanthin in halibut is higher than that in Atlantic salmon, possibly due to the lower feed intake of halibut and its stronger astaxanthin metabolic conversion capacity, resulting in a lower astaxanthin retention rate. This study aimed to investigate the metabolism of astaxanthin (Ax) in Atlantic salmon, especially its liver. Live salmon were used in this study and fed a diet containing 60 ppm of 15,15'(14)C-labeled astaxanthin before sacrifice. Blood, bile, liver, gastrointestinal tract and its contents, muscle, skin, remaining carcass, and fecal samples were collected for scintillation counting. At the end of the experiment, the highest radioactivity of 14C-labeled Ax was detected in gastrointestinal contents and feces (71.36%), 7.13% in bile, and 10.68% in liver, muscle, and skin samples. Metabolites of 14C-labeled Ax were extracted from salmon bile and analyzed using thin-layer chromatography (TLC) and high-performance liquid chromatography (HPLC). The results showed that the main components were 14C-labeled Ax and its cis isomers, and no 14C-labeled Ax conjugates were observed. These results indicate that (14)C-labeled astaxanthin does not bind to larger colorless compounds in Atlantic salmon liver. Metabolites/Metabolites Eight adult female rainbow trout were fed a forced-feed meal containing labeled (14)C-astaxanthin and (3)H-canthaxanthin or (3)H-zeaxanthin. Ninety-six hours after feeding, rainbow trout were euthanized, and their livers, skin, muscles, and ovaries were dissected. Astaxanthin accumulated slightly more in the muscles than canthaxanthin, but in all tissues, the concentrations of both astaxanthin and canthaxanthin were significantly higher than those of zeaxanthin. Metabolites of (3)H-zeaxanthin were found only in the liver, while (14)C-zeaxanthin was the only detected (14)C-astaxanthin metabolite present in all tissues examined. The presence of (3)H-astaxanthin in the livers of all trout suggests that (3)H-canthaxanthin and (3)H-zeaxanthin are precursors to astaxanthin, and that salmonids may possess previously unknown carotenoid oxidation pathways. Labeled retinol 1 and retinol 2 were detected only in the liver, with (3)H-zeaxanthin being the major precursor to both forms of vitamin A. This study determined the effects of feed intake, growth rate, and temperature (8°C and 12°C) on the apparent digestibility coefficient (ADC) of Atlantic salmon, the absorption of various astaxanthin E/Z isomers in blood, and the metabolism of astaxanthin (3,3'-dihydroxy-β,β-carotene-4,4'-dione). The accumulation of iodoflavin (3,4,3'-trihydroxy-β,β-carotene-4-one) in plasma was used to indicate the metabolic transformation of astaxanthin.

Interactions
This study investigated the in vivo protective effect of astaxanthin, isolated from a mutant of Xanthophyllomyces dendrorhous, against ethanol-induced gastric mucosal injury in rats. Experimental rats were pretreated with two doses of astaxanthin (5 and 25 mg/kg body weight, respectively) for 3 days, followed by 3 days of treatment with 80% ethanol; control rats received only 80% ethanol treatment for 3 days. Results showed that oral administration of astaxanthin (5 and 25 mg/kg body weight) significantly reduced ethanol-induced gastric mucosal injury and inhibited the increase in gastric mucosal lipid peroxide levels. Furthermore, astaxanthin pretreatment significantly increased the activities of free radical scavenging enzymes such as superoxide dismutase, catalase, and glutathione peroxidase. Histological examination clearly demonstrated that ethanol-induced acute gastric mucosal injury almost disappeared after astaxanthin pretreatment.

[1]. Anti-Tumor Effects of Astaxanthin by Inhibition of the Expression of STAT3 in Prostate Cancer. Mar Drugs. 2020 Aug 7;18(8):415.

[2]. Effect of astaxanthin on retinal pigment epithelial cells in high glucose: an in-vitro study. Biomed Res, 2017, 28(15): 6839-6843.

[3]. Carotenoids inhibit proliferation and regulate expression of peroxisome proliferators-activated receptor gamma (PPARγ) in K562 cancer cells. Arch Biochem Biophys. 2011 Aug 1;512(1):96-106.

[4]. Seven day oral supplementation with Cardax (disodium disuccinate astaxanthin) provides significant cardioprotection and reduces oxidative stress in rats. Mol Cell Biochem. 2006 Feb;283(1-2):23-30.

[5]. Multiple Mechanisms of Anti-Cancer Effects Exerted by Astaxanthin. Mar Drugs. 2015 Jul 14;13(7):4310-30.

Astaxanthin is a carotenoid ketone composed of β,β-carotene-4,4'-dione, with two hydroxyl groups attached to the 3 and 3' positions respectively (3S,3'S diastereomers). It is a carotenoid pigment primarily found in animals (crustaceans, echinoderms), but also in plants. Astaxanthin can exist in free form (as a red pigment), ester form, or as a blue, brown, or green pigment protein. It possesses various functions, including anticoagulation, antioxidant activity, food coloring, and as a plant and animal metabolite. It is both a carotenoid ketone and a carotene alcohol, derived from the hydrogenation of β-carotene. Astaxanthin is a ketone carotenoid belonging to the terpenoid family. While classified as lutein, it is actually a carotenoid lacking vitamin A activity. It is found in most aquatic organisms with red pigments. Astaxanthin has been shown to have antioxidant and anti-inflammatory effects. It may be present as a coloring agent in fish feed or some animal feeds. Astaxanthin has been reported to be found in Agrobacterium aurantiacum, Phaffia rhodozyma, and other organisms with relevant data. Astaxanthin is a natural and synthetic lutein compound, belonging to the non-provitamin A carotenoid family, and possesses potential antioxidant, anti-inflammatory, and antitumor activities. After ingestion, astaxanthin acts as an antioxidant, reducing oxidative stress and thus preventing protein and lipid oxidation as well as DNA damage. By reducing the production of reactive oxygen species (ROS) and free radicals, it can also prevent ROS-induced activation of the nuclear factor κB (NF-κB) transcription factor and the production of inflammatory cytokines such as interleukin-1β (IL-1β), IL-6, and tumor necrosis factor-α (TNF-α). Furthermore, astaxanthin may inhibit the activity of cyclooxygenase-1 (COX-1) and nitric oxide (NO), thereby alleviating inflammation. Oxidative stress and inflammation play key roles in the pathogenesis of various diseases, including cardiovascular diseases, neurological diseases, autoimmune diseases, and oncological diseases.

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Pharmaceutical Indications
It has been investigated for the treatment of eye diseases/infections, cancer/tumors (not specified), and asthma.

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Therapeutic Use
This study hypothesizes that oral administration of Cadax (disuccinate disodium astaxanthin) can inhibit oxidative damage to multiple relevant biological targets in a representative, well-defined mouse peritoneal inflammation model. Using previously developed mass spectrometry (LC/ESI/MS/MS) based methods, multiple different oxidative pathways were detected in a black mouse (C57/BL6) model system. Mice were treated with Cardax or a carrier (a drug-free lipophilic emulsion) at a dose of 500 mg/kg once daily for 7 consecutive days. On day 8, in vivo oxidative stress markers in peritoneal lavage fluid samples (supernatant) were assessed at five time points: (1) baseline before treatment (t=0); (2) intraperitoneal injection of thioglycolate 16 hours to induce neutrophil infiltration; (3) intraperitoneal injection of yeast cell wall (yeast polysaccharide; t=16 h/4 h thioglycolate + yeast polysaccharide) 4 hours later; (4) intraperitoneal injection of thioglycolate 72 hours to induce monocyte/macrophage infiltration; and (5) 72 h/4 h thioglycolate + yeast polysaccharide. Statistically significant sparing effects on arachidonic acid (AA) and linoleic acid (LA) substrates were observed at the second and fifth time points. After normalization to the concentration of the oxidizing substrate, a statistically significant decrease in 8-isoprostan-F(2α) (8-iso-F(2α)) was observed at the third time point (when neutrophil recruitment/activation reached its maximum), and statistically significant decreases in 5-HETE, 5-oxo-EET, 11-HETE, 9-HODE, and PGF(2α) were observed at the fifth time point (when monocyte/macrophage recruitment/activation reached its maximum). Subsequently, we evaluated the direct interaction between the optically inactive stereoisomer of Cardax (meso-dAST) and human 5-lipoxygenase (5-LOX) in vitro using circular dichroism (CD) and UV/Vis absorption spectroscopy, and performed subsequent molecular docking calculations using mammalian 15-LOX as a substitute (X-ray fluorescence spectroscopy data have been reported). The results indicate that this meso compound can interact with and bind to the solvent-exposed surface of the enzyme. These preliminary studies lay the foundation for a more detailed evaluation of the therapeutic effects of this compound on 5-LOX enzymes, which play an important role in human chronic diseases such as atherosclerosis, asthma, and prostate cancer. /Disuccinate astaxanthin/
The composition of atherosclerotic plaques, not just the size of macroscopic lesions, is related to their susceptibility to rupture and the risk of thrombosis. This study evaluated the potential anti-atherosclerotic effects of the antioxidants α-tocopherol and astaxanthin in Watanabe hereditary hyperlipidemia (WHHL) rabbits by focusing on lipid quality, macrophages, apoptosis, collagen, metalloproteinase expression, and plaque integrity. Thirty-one WHHL rabbits were divided into three groups and fed a standard diet (control group, n=10), a standard diet supplemented with 500 mg/kg α-tocopherol (n=11), or a standard diet supplemented with 100 mg/kg astaxanthin (n=10) for 24 weeks. The results showed that both antioxidants, especially astaxanthin, significantly reduced macrophage infiltration in plaques, but had no effect on lipid accumulation. Based on the distribution of collagen and smooth muscle cells, all lesions in the astaxanthin-treated rabbits were classified as early plaques. Both antioxidants improved plaque stability and significantly reduced apoptosis, which mainly occurred in macrophages, while also reducing matrix metalloproteinase 3 expression and plaque rupture. Although neither antioxidant altered the positive correlation between lesion size and lipid accumulation, lesion size was positively correlated with apoptosis only in the control group. Astaxanthin and α-tocopherol may improve the stability of atherosclerotic plaques by reducing macrophage infiltration and apoptosis. The reduction in apoptosis by α-tocopherol and astaxanthin may be a novel anti-atherosclerotic property of these antioxidants.
Experimental Treatment: Astaxanthin is a carotenoid without vitamin A activity and may exert anti-tumor activity by enhancing the immune response. This study aimed to investigate the effects of dietary astaxanthin on the growth and tumor immunity of transplanted methylcholanthrene-induced fibrosarcoma (Meth-A tumor) cells. These tumor cells express a tumor antigen that induces a T-cell-mediated immune response in syngeneic mice. BALB/c mice were fed a chemically defined diet supplemented with astaxanthin (0.02%, 40 μg/kg body weight/day, in microbeads) for 0, 1, and 3 weeks prior to subcutaneous inoculation with tumor cells (3 × 10⁵ cells, 2 times the minimum tumorigenic dose). Tumor size and weight were measured 3 weeks after inoculation. We also measured cytotoxic T lymphocyte (CTL) activity and interferon-γ (IFN-γ) production by restimulating tumor draining lymph nodes (TDLN) and spleen cells with Meth-A tumor cells in vitro. Mice supplemented with astaxanthin at 1 and 3 weeks prior to tumor inoculation showed significantly smaller tumor size and weight compared to the control group. This antitumor activity paralleled the higher CTL activity and IFN-γ production levels in the tumor draining lymph nodes (TDLN) and spleen cells of mice fed with astaxanthin. Mice fed astaxanthin three weeks prior to tumor inoculation exhibited the highest CTL activity in their TDLN cells. When astaxanthin supplementation was initiated concurrently with tumor inoculation, dietary astaxanthin had no effect on the aforementioned parameters except for IFN-γ production in splenocytes. After four weeks of feeding mice with 0.02% astaxanthin, the serum total astaxanthin concentration was approximately 1.2 μmol/L, and appeared to increase with prolonged astaxanthin supplementation. Our results indicate that dietary astaxanthin inhibits the growth of Meth-A tumor cells and stimulates an immune response against Meth-A tumor antigens.
Experimental Treatment: In this study, we evaluated the potential role of a synthetic astaxanthin derivative (Cardax; disodium astaxanthin succinate) as a cardioprotective agent by leveraging its improved oral bioavailability. We administered astaxanthin as a dietary supplement to Sprague-Dawley rats for 7 days via a subchronic oral administration route. Animals were fed either two concentrations of Cardax (0.1% and 0.4%; approximately 125 and 500 mg/kg/day, respectively) or a control diet without the drug for 7 days. Infarction was studied on day 8. The left anterior descending (LAD) coronary artery was occluded for 30 minutes, followed by reperfusion for 2 hours, and then the animals were sacrificed. This protocol resulted in a mean infarct area (IS) as a percentage of the area at risk (AAR) (IS/AAR, %) of 61 ± 1.8%. AAR was quantified by injection of patent blue dye, and IS was determined by staining with triphenyltetrazolium chloride (TTC). After 7 days of dietary supplementation with 0.1% and 0.4% Cardax, the mean IS/AAR (%) significantly decreased to 45 ± 2.0% (26% salvage rate) and 39 ± 1.5% (36% salvage rate), respectively. After 7 days of supplementation with two concentrations of astaxanthin (400±65 nM and 1634±90 nM, respectively), the concentration of free astaxanthin in the myocardium reached ideal levels, indicating excellent loading capacity in target organs of solid tissues after oral supplementation. Simultaneously, plasma levels of various lipid peroxidation products were observed to decrease after supplementation with disodium astaxanthin succinate, consistent with the reported in vitro antioxidant mechanism. These results suggest that the potential cardioprotective value of this compound has been extended to patients undergoing elective cardiovascular surgery, for whom 7 days of oral pretreatment (similar to statins) can significantly reduce perioperative induced myocardial infarction area. (Disodium astaxanthin succinate)
For more complete data on the therapeutic uses of astaxanthin (7 types), please visit the HSDB record page.

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Astaxanthin is a natural carotenoid found in algae, phytoplankton, and marine organisms such as shrimp. [1]
Studies have shown that astaxanthin inhibits the proliferation, colony formation, migration, and invasion of invasive prostate cancer DU145 cells and promotes their apoptosis, mainly by reducing the expression levels of STAT3 protein and mRNA. [1]
In in vitro and in vivo models, the antitumor effect of astaxanthin is synergistic with STAT3 gene silencing (si-STAT3). [1]
The authors propose that astaxanthin is a potential natural product that can be used to inhibit invasive prostate cancer cells. [1]

C40H52O4

596.8385

596.386

472-61-7

5281224

Dark purple to black solid powder

1.1±0.1 g/cm3

774.0±60.0 °C at 760 mmHg

215-216ºC

435.8±29.4 °C

0.0±6.0 mmHg at 25°C

1.595

8.16

2

4

10

44

1340

2

CC1=C(C(C[C@@H](C1=O)O)(C)C)/C=C/C(=C/C=C/C(=C/C=C/C=C(/C=C/C=C(/C=C/C2=C(C(=O)[C@H](CC2(C)C)O)C)\C)\C)/C)/C

MQZIGYBFDRPAKN-UWFIBFSHSA-N

InChI=1S/C40H52O4/c1-27(17-13-19-29(3)21-23-33-31(5)37(43)35(41)25-39(33,7)8)15-11-12-16-28(2)18-14-20-30(4)22-24-34-32(6)38(44)36(42)26-40(34,9)10/h11-24,35-36,41-42H,25-26H2,1-10H3/b12-11+,17-13+,18-14+,23-21+,24-22+,27-15+,28-16+,29-19+,30-20+/t35-,36-/m0/s1

(6S)-6-Hydroxy-3-[(1E,3E,5E,7E,9E,11E,13E,15E,17E)-18-[(4S)-4-hydroxy-2,6,6-trimethyl-3-oxo-1-cyclohexenyl]-3,7,12,16-tetramethyloctadeca-1,3,5,7,9,11,13,15,17-nonaenyl]-2,4,4-trimethyl-1-cyclohex-2-enone

Astaxanthin

2934.99.9001

Powder      -20°C    3 years

                     4°C     2 years

In solvent   -80°C    6 months

                  -20°C    1 month

Note: (1). This product requires protection from light (avoid light exposure) during transportation and storage.  (2). Please store this product in a sealed and protected environment (e.g. under nitrogen), avoid exposure to moisture.  (3). This product is not stable in solution, please use freshly prepared working solution for optimal results.

Room temperature (This product is stable at ambient temperature for a few days during ordinary shipping and time spent in Customs)

DMSO : ~2 mg/mL (~3.35 mM)
Acetone :< 1 mg/mL

Solubility in Formulation 1: 3.33 mg/mL (5.58 mM) in 0.5% CMC-Na/saline water (add these co-solvents sequentially from left to right, and one by one), suspension solution; with heating and sonication.
Preparation of saline: Dissolve 0.9 g of sodium chloride in 100 mL ddH₂ O to obtain a clear solution.

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Solubility in Formulation 2: 3.33 mg/mL (5.58 mM) in 20% HP-β-CD in Saline (add these co-solvents sequentially from left to right, and one by one), suspension solution; with heating and sonication.
Preparation of saline: Dissolve 0.9 g of sodium chloride in 100 mL ddH₂ O to obtain a clear solution.

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 (Please use freshly prepared in vivo formulations for optimal results.)