Atorvastatin calcium trihydrate is the trihydrate form of atorvastatin calcium.

Take only under medical supervision. 

Atorvastatin, a member of the statin family and one of the statin class inhibitors, is a lipidic agent that lowers levels of 3-hydroxy-3-methylgutaryl-CoA (HMG-CoA) reductase, so as to reduce elevated level of low density lipoproteins (LDL) cholesterol and cardiovascular risk.

In addition to its anti-cholesterol properties, atorvastatin has been shown to suppress the proliferation of cancer cells and induce apoptosis (1) and also playing a role in immunosuppression, fighting inflammation (there is a close association between inflammation and tumor), preventing dementia.

However, it has a problem of scarce gastric solubility and low total bioavailability together with higher pre-system clearance.

It has also demonstrated an antifungal ability against Candida albicans in vivo and in vitro (2).

in this study atorvastatin demonstrated positive effects on erectile function after radical prostatectomy surgery (3).

It also limited the influenza virus to generate lipid droplets and greatly suppresses virus replication (4).

Like all drugs it can cause side effects. Always consult your doctor.

Atorvastatin studies

Molecular  Formula: C₆₆H₇₄CaF₂N₄O₁₃

Molecular Weight: 1209.4 g/mol

CAS:  344423-98-9  1035205-53-8  1574495-40-1

NACRES NA.24

Sinonimi:

• Totalip
• Torvast
• Calcium (3R,5R)-7-(2-(4-fluorophenyl)-5-isopropyl-3-phenyl-4-(phenylcarbamoyl)-1H-pyrrol-1-yl)-3,5-dihydroxyheptanoate trihydrate
• 1H-Pyrrole-1-heptanoic acid, 2-(4-fluorophenyl)-beta,delta-dihydroxy-5-(1-methylethyl)-3-phenyl-4-((phenylamino)carbonyl)-, calcium salt (2:1), trihydrate, (betaR,deltaR)-
• calcium (3R,5R)-7-[2-(4-fluorophenyl)-3-phenyl-4-(phenylcarbamoyl)-5-propan-2-ylpyrrol-1-yl]-3,5-dihydroxyheptanoate trihydrate
• calcium bis{(3R,5R)-7-[3-(anilinocarbonyl)-5-(4-fluorophenyl)-2-isopropyl-4-phenyl-1H-pyrrol-1-yl]-3,5-dihydroxyheptanoate} trihydrate

References___________________________________________________

(1)   Yuan Q, Dong CD, Ge Y, Chen X, Li Z, Li X, Lu Q, Peng F, Wu X, Zhao J, Liu K. Proteome and phosphoproteome reveal mechanisms of action of atorvastatin against esophageal squamous cell carcinoma. Aging (Albany NY). 2019 Nov 7;11. doi: 10.18632/aging.102402.

Abstract. Statins comprise a class of prescription drugs used for reducing cholesterol. Evidence has also showed that statins could reduce cancer incidence. However, the anti-tumor mechanism of statins has not been fully defined. Here, we found that atorvastatin inhibited proliferation of esophageal squamous cell carcinoma (ESCC) cells. The underlying mechanisms were explored by mass spectrometry. The proteome data revealed that atorvastatin inhibited the cAMP and Rap1 signal pathways, except for Ras signal pathway. Interestingly, phosphoproteome profiles suggested that ERKT185/Y187, CDK1T14, and BRAC1S1189 phosphorylation-mediated Th17 cell differentiation, Gap junction and the Platinum drug resistance pathway were down-regulated after atorvastatin treatment. The phosphorylation levels of ERKT185/Y187, CDK1T14 and BRAC1S1189 were confirmed by western blotting in KYSE150 cells. More importantly, atorvastatin suppresses ESCC tumor growth in PDX models. The molecular changes in tumor tissues were confirmed by immunohistochemistry. In conclusion, deep-proteome and phosphoproteome analysis reveal a comprehensive mechanism that contributes to atorvastatin's anti-tumor effect.

(2) Ajdidi A, Sheehan G, Abu Elteen K, Kavanagh K. Assessment of the in vitro and in vivo activity of atorvastatin against Candida albicans.  J Med Microbiol. 2019 Oct;68(10):1497-1506. doi: 10.1099/jmm.0.001065.

Abstract. Aim. The aim of this work was to characterize the response of Candida albicans to atorvastatin, and to assess its in vivo antifungal capability.Methodology. The effect of atorvastatin on the growth and viability of C. albicans was assessed. The ability of the statin to alter cell permeability was quantified by measuring amino acid and protein leakage. The response of C. albicans to atorvastatin was assessed using label-free quantitative proteomics. The in vivo antifungal activity of atorvastatin was assessed using Galleria mellonella larvae infected with C. albicans.Results. Atorvastatin inhibited the growth of C. albicans. The atorvastatin-treated cells showed lower ergosterol levels than the controls, demonstrated increased calcofluor staining and released elevated quantities of amino acids and protein. Larvae infected with C. albicans showed a survival rate of 18.1±4.2 % at 144 h. In contrast, larvae administered atorvastatin (9.09 mg kg-1) displayed a survival rate of 60.2±6.4 % (P<0.05). Label-free quantitative proteomics identified 1575 proteins with 2 or more peptides and 465 proteins were differentially abundant (P<0.05). There was an increase in the abundance of enzymes with oxidoreductase and hydrolase activity in atorvastatin-treated cells, and squalene monooxygenase (4.52-fold increase) and lanosterol synthase (2.84-fold increase) were increased in abundance. Proteins such as small heat shock protein 21 (-6.33-fold) and glutathione peroxidase (-2.05-fold) were reduced in abundance.Conclusion. The results presented here indicate that atorvastatin inhibits the growth of C. albicans and is capable of increasing the survival of G. mellonella larvae infected with C. albicans.

(3)   Siltari A, Riikonen J, Fode M, Murtola TJ. Effects of Preoperative Atorvastatin Treatment On Erectile Function After Radical Prostatectomy: Results From a Subgroup of ESTO1, a Randomized, Double-Blind, Placebo-Controlled Study. J Sex Med. 2019 Oct;16(10):1597-1605. doi: 10.1016/j.jsxm.2019.07.001

(4) Episcopio D, Aminov S, Benjamin S, Germain G, Datan E, Landazuri J, Lockshin RA, Zakeri Z. Atorvastatin restricts the ability of influenza virus to generate lipid droplets and severely suppresses the replication of the virus.   FASEB J. 2019 Aug;33(8):9516-9525. doi: 10.1096/fj.201900428RR.

Abstract. Influenza virus causes infected cells to generate large numbers of lipid droplets. Because the virus envelope contains substantial cholesterol, we applied atorvastatin (ATV) to Madin-Darby Canine Kidney cells before infecting them. Five micromolars ATV, within physiologic range, strongly (>95%) inhibits reproduction of influenza A as measured by PCR of viral RNA, plaque assay for viable virus, and production of virus nucleoprotein (NP). Inhibition of any of the following can suppress formation of lipid droplets (>-50%) but does not interfere with the production of NP: endoplasmic reticulum stress, autophagy, or production of reactive oxygen substances (ROS). We conclude that, regardless of whether this widely used statin, which is generally considered to be safe, can prevent infection or minimize its severity, inhibition of the 3-hydroxy-3-methylglutaryl-coenzyme A reductase pathway to protect against infection by influenza virus or to mitigate its severity warrants further exploration.-Episcopio, D., Aminov, S., Benjamin, S., Germain, G., Datan, E., Landazuri, J., Lockshin, R. A., Zakeri, Z. Atorvastatin restricts the ability of influenza virus to generate lipid droplets and severely suppresses the replication of the virus.