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Composition of Proprietary Products Approved in the United States
Published in Sarfaraz K. Niazi, Handbook of Pharmaceutical Manufacturing Formulations, Third Edition, 2019
Diovan HCT® (valsartan and hydrochlorothiazide, USP) tablets are formulated for oral administration to contain valsartan and hydrochlorothiazide, USP 80/12.5 mg, 160/12.5 mg, and 160/25 mg. The inactive ingredients of the tablets are colloidal silicon dioxide, crospovidone, hydroxypropyl methylcellulose, iron oxides, magnesium stearate, microcrystalline cellulose, polyethylene glycol, talc, and titanium dioxide.
Clinical Effects of Pollution
Published in William J. Rea, Kalpana D. Patel, Reversibility of Chronic Disease and Hypersensitivity, Volume 5, 2017
William J. Rea, Kalpana D. Patel
The precise role of autophagy regulation contributing to cell survival and death in ischemic hearts remains controversial. Xie and colleagues620 report that suberoylanilide hydroxamic acid (SAHA; vorinostat), a histone deacetylase (HDAC) inhibitor approved by the Food and Drug Administration for cancer treatment, attenuated myocardial reperfusion injury in rabbits. These results revealed that SAHA reduced infarct size and partially rescued systolic function when administered either before surgery or at the time of reperfusion. SAHA was found to facilitate autophagic flux in the infarct border zone in rabbit myocardium and in mice harboring a red fluorescent protein–free fluorescent protein–LC3 transgene. In cultured myocytes subjected to I/R, SAHA overtly alleviated cell death, the effect of which was correlated with increased autophagy. The permissive role of autophagy in SAHA-related beneficial effects was consolidated by the mitigation of SAHA efficacy through RNAi knockdown of autophagy genes Atg7 and Atg5. These findings have great clinical relevance because the plasma SAHA levels were similar to those achieved in cancer patients.620 This work has unveiled a new paradigm for the clinical utility of HDAC inhibitors and autophagy regulators in IHDs. A plethora of studies have demonstrated proven cardioprotective benefits of HDAC inhibitors in models of myocardial stress, including cardiac hypertrophy I/R and heart failure.621–623 In particular, trichostatin A, a class I and II HDAC inhibitor structurally homologous to SAHA, reduced myocardial infarct size up to 50%.624 HDAC inhibition caused a dramatic increase in phosphorylation of p38 and p38 activity in the heart.624 Of note, HDAC inhibitors can be delivered as late as 1 hour after an ischemic insult and can achieve a similar degree of infarct size reduction using pretreatment, indicating the suitability of HDAC inhibitors to treat MI at the time of percutaneous coronary intervention. Although discrepancies exist in disease mechanisms in animal models relative to the human case, these data clearly show that facilitated autophagy is required for HDAC inhibition–induced protection against I/R injury.620 Given the recent therapeutic promises using HDAC inhibitors in ischemic and hypertrophic heart diseases,621,622,625,626 the finding that SAHA rescues I/R heart injury through modulating autophagy flux is of great clinical importance. Interestingly, a number of cardioprotective agents such as the angiotensin II receptor blocker valsartan may also elicit protection against I/R injury through autophagy induction. Valsartan preconditioning is believed to facilitate autophagy induction via an Akt/mammalian target of rapmycin/S6K-mediated mechanism, although the underlying molecular mechanism behind SAHA-induced autophagy flux remains unclear at this time.
Improved transdermal delivery of valsartan using combinatorial approach of polymeric transdermal hydrogels and solid microneedles: an ex vivo proof of concept investigation
Published in Journal of Biomaterials Science, Polymer Edition, 2023
Cindy Kristina Enggi, Mega Tri Satria, Nirmayanti Nirmayanti, Jesscia Theodor Usman, Julika Fajrika Nur, Rangga Meidianto Asri, Nana Juniarti Natsir Djide, Andi Dian Permana
Valsartan (VAL) is an antihypertensive drug which belongs to angiotensin II receptor blocker (ARB). The use of VAL does not associate with persistent cough/angioedema due to its ability to not inhibit the breakdown of bradykinin. According to Nixon et al. [5], among other ARB drugs, VAL is found to be more effective at lowering BP and shows comparable efficacy in patients. However, when administrated orally, VAL exhibits low bioavailability (around 10–35%) due to poor absorption in the gastrointestinal tract. Furthermore, food intake is known to affect the pharmacokinetics of VAL by reducing its Cmax and AUC [6, 7]. Therefore, finding an alternative route for delivering VAL is needed.