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Fig. 1 · Structure
Cat. No.
A11123
CAS No.
173334-58-2
Formula
C30H53N3O6.1/2C4H4O4
Mol. Weight
609.8

Documents & Downloads

Aliskiren hemifumarate

Cat. No. A11123 CAS 173334-58-2

renin inhibitor

Aliskiren hemifumarate is a hemifumarate salt form of Aliskiren, which is a direct renin inhibitor approved for the treatment of essential hypertension.

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Biological Activity

Target & Activity

Target Activity Value
Renin 1.5 nM

In Vivo Studies

In male spontaneously hypertensive rats, powdered Aliskiren administered by gavage did not affect the gene expression studied and decreased NADPH oxidase protein expression compared with untreated rats. In male Swiss albino mice with STZ-induced diabetes, daily oral Aliskiren significantly lowered fasting blood glucose compared with the STZ-only treated group. In male mice, cardiomyocyte cross-sectional diameter was similar across groups, including those receiving hyperhomocysteinemia-inducing diets with or without Aliskiren administered via osmotic mini-pump. [1,2,3]

Literature-reported observations and conditions; not Adooq-tested protocols or general treatment recommendations.

Aliskiren and gene expression in hypertensive rats

Animal study · Male, 12-week-old spontaneously hypertensive rats; six animals [1]

Male spontaneously hypertensive rats received powdered aliskiren via gavage. Compared with the untreated group, treatment did not affect any gene expression studied.

Measured endpoints — not treatment concentrations
EndpointReported resultReference
gene expression of atp6ap2, agtr1, and ACEReported result The powdered form of aliskiren did not affect any gene expression studied[1]

Conditions shared by the study groups

Route
via gavage
Treatment course
for 3 weeks
Study groups and reported outcomes
Group / doseComparatorObserved resultReference
Aliskiren 25 mg/kg/dayuntreated group (SHR)The powdered form of aliskiren did not affect any gene expression studied[1]
Aliskiren 25 mg/kg/day
Model: Male, 12-week-old spontaneously hypertensive rats; six animals
Reported limits: Not stated in the sentences used: vehicle.
Methods and source locations

Compound reported in the paper: Aliskiren

The paper names Aliskiren without stating the salt or form; not verified as the hemifumarate form supplied as A11123. No dose conversion or lot validation.

2. Results > 2.4. Profiling of Gene Expression (S8); 4. Materials and Methods > 4.3. Animals and Treatment (S33, S34, S35, S39)

gene expression of atp6ap2, agtr1, and ACE: gene expression of atp6ap2, agtr1, and ACE; comparator: untreated group (SHR) — 2. Results > 2.4. Profiling of Gene Expression (S8); 4. Materials and Methods > 4.3. Animals and Treatment (S39)

Aliskiren 25 mg/kg/day · 2. Results > 2.4. Profiling of Gene Expression (S8); 4. Materials and Methods > 4.3. Animals and Treatment (S33, S35)

Aliskiren and Blood Glucose in Diabetic Mice

Animal study · Male Swiss albino mice; STZ-induced diabetic mice; 8 mice each [2]

In male Swiss albino mice with STZ-induced diabetes, daily oral Aliskiren significantly lowered fasting blood glucose compared with the STZ-only treated group.

Measured endpoints — not treatment concentrations
EndpointReported resultReference
Fasting blood glucoseBlood glucose daily aliskiren (25 mg /kg oral, dissolved in sterile normal saline) for 1 month: 161 ± 15.4 mg/dl[2]

Conditions shared by the study groups

Route
oral
Treatment course
three days after STZ injection; daily aliskiren; for 1 month
Vehicle
sterile normal saline
Study groups and reported outcomes
Group / doseComparatorObserved resultReference
Aliskiren 25 mg /kgdiabetic control group (STZ-induced diabetic mice and received normal saline, IP, for 1 month)significant lowering in blood glucose; 161 ± 15.4 mg/dl; P < 0.05[2]
Aliskiren 25 mg /kg
Model: Male Swiss albino mice; STZ-induced diabetic mice; 8 mice each
Methods and source locations

Compound reported in the paper: Aliskiren

The paper names Aliskiren without stating the salt or form; not verified as the hemifumarate form supplied as A11123. No dose conversion or lot validation.

Methods > Animals and experimental design (S1, S2, S3); Methods > Diabetes induction (S8); Methods > Biochemical analysis > Blood glucose and serum insulin (S17); Results > Blood glucose and serum insulin level (S46); Table 1 (T1.h1, T1.r3)

Fasting blood glucose: Fasting blood glucose; comparator: diabetic control group (STZ-induced diabetic mice and received normal saline, IP, for 1 month) — Methods > Animals and experimental design (S3); Methods > Biochemical analysis > Blood glucose and serum insulin (S17); Results > Blood glucose and serum insulin level (S46); Table 1 (T1.h1, T1.r3)

Aliskiren 25 mg /kg · Methods > Animals and experimental design (S3); Results > Blood glucose and serum insulin level (S46); Table 1 (T1.h1, T1.r3)

Aliskiren and Cardiomyocyte Size in Mice

Animal study · Male C57BL6 mice (8–10 weeks old) [3]

In male mice receiving hyperhomocysteinemia-inducing diets, Aliskiren was administered via osmotic mini-pump. Cardiomyocyte cross-sectional diameter was similar across groups, including the hyperhomocysteinemia group and groups receiving hyperhomocysteinemia-inducing diets plus Aliskiren.

Measured endpoints — not treatment concentrations
EndpointReported resultReference
Cardiomyocyte size estimated as cross-sectional diameterCardiomyocyte size Hhe + aliskiren 0.5 mg/kg/day: 16.7±0.8 µm; Hhe + aliskiren 5 mg/kg/day: 16.1±0.8 µm; Hhe + aliskiren 50 mg/kg/day: 16.3±0.6 µm[3]

Conditions shared by the study groups

Route
via osmotic mini-pump
Treatment course
12 weeks
Study groups and reported outcomes
Group / doseComparatorObserved resultReference
Aliskiren 0.5 mg/kg/day, 5 mg/kg/day, or 50 mg/kg/dayHhe: 16.4±0.8 µmCardiomyocyte size estimated as cross-sectional diameter was similar between groups (Control: 16±0.4 µm; Hhe: 16.4±0.8 µm; Hhe + aliskiren 0.5 mg/kg/day: 16.7±0.8 µm; Hhe + aliskiren 5 mg/kg/day: 16.1±0.8 µm; and Hhe + aliskiren 50 mg/kg/day: 16.3±0.6 µm).[3]
Aliskiren 0.5 mg/kg/day, 5 mg/kg/day, or 50 mg/kg/day
Model: Male C57BL6 mice (8–10 weeks old)
Reported limits: Not stated in the sentences used: vehicle.
Methods and source locations

Compound reported in the paper: Aliskiren

The paper names Aliskiren without stating the salt or form; not verified as the hemifumarate form supplied as A11123. No dose conversion or lot validation.

Materials and Methods > Animal model (S3, S5, S7, S8, S11); Results > Effects of aliskiren on cardiac hypertrophy, blood pressure and RAS (S47)

Cardiomyocyte size estimated as cross-sectional diameter: Cardiomyocyte size estimated as cross-sectional diameter; comparator: Hhe: 16.4±0.8 µm — Results > Effects of aliskiren on cardiac hypertrophy, blood pressure and RAS (S47)

Aliskiren 0.5 mg/kg/day, 5 mg/kg/day, or 50 mg/kg/day · Materials and Methods > Animal model (S5, S8, S11); Results > Effects of aliskiren on cardiac hypertrophy, blood pressure and RAS (S47)

Aliskiren and NADPH Oxidase Expression in Hypertensive Rats

Animal study · Male, 12-week-old spontaneously hypertensive rats; six animals [1]

Male, 12-week-old spontaneously hypertensive rats; powdered aliskiren at a dose of 25 mg/kg/day. The treatment was administered via gavage for 3 weeks; aliskiren decreased the protein expression of NADPH oxidase.

Measured endpoints — not treatment concentrations
EndpointReported resultReference
protein expression of NADPH oxidaseReported result powdered aliskiren at a dose of 25 mg/kg/day: decreased the protein expression of NADPH oxidase[1]

Conditions shared by the study groups

Route
via gavage
Treatment course
for 3 weeks
Study groups and reported outcomes
Group / doseComparatorObserved resultReference
Aliskiren 25 mg/kg/dayuntreated group (SHR)powdered aliskiren at a dose of 25 mg/kg/day: decreased the protein expression of NADPH oxidase[1]
Aliskiren 25 mg/kg/day
Model: Male, 12-week-old spontaneously hypertensive rats; six animals
Reported limits: Not stated in the sentences used: vehicle.
Methods and source locations

Compound reported in the paper: Aliskiren

The paper names Aliskiren without stating the salt or form; not verified as the hemifumarate form supplied as A11123. No dose conversion or lot validation.

2. Results > 2.5. Protein Expression of NADPH Oxidase and Concentration of Conjugated Diene (S9); 4. Materials and Methods > 4.3. Animals and Treatment (S33, S34, S35, S40); Figure 4 legend (S84)

protein expression of NADPH oxidase: protein expression of NADPH oxidase; comparator: untreated group (SHR) — 2. Results > 2.5. Protein Expression of NADPH Oxidase and Concentration of Conjugated Diene (S9); 4. Materials and Methods > 4.3. Animals and Treatment (S33, S40)

Aliskiren 25 mg/kg/day · 2. Results > 2.5. Protein Expression of NADPH Oxidase and Concentration of Conjugated Diene (S9); 4. Materials and Methods > 4.3. Animals and Treatment (S33, S35)

Specifications

Manufacturer Adooq Bioscience
Actions Inhibitor
CAS Number 173334-58-2
Applications renin inhibitor
Formula C30H53N3O6.1/2C4H4O4
Molecular Weight 609.8
SMILES
CC(C)[C@@H](CC1=CC(=C(C=C1)OC)OCCCOC)C[C@@H]([C@H](C[C@@H](C(C)C)C(=O)NCC(C)(C)C(=O)N)O)N.CC(C)[C@@H](CC1=CC(=C(C=C1)OC)OCCCOC)C[C@@H]([C@H](C[C@@H](C(C)C)C(=O)NCC(C)(C)C(=O)N)O)N.C(=C/C(=O)O)\C(=O)O

Storage & Solubility

In Vitro Solubility

Reported Solubility

SolventReported Solubility
DMSO 89 mg/mL (145.94 mM)
Water 89 mg/mL (145.94 mM)
Ethanol 89 mg/mL (145.94 mM)

Preparing Stock Solutions

Stock preparation is unavailable for this product molecular weight.

Calculated stock concentrations do not establish solvent solubility. Refer to the reported solubility data for experimental guidance.

Storage

Store powder at -20°C, keep desiccated.
In powder form, the chemical is stable for 36 months.
In solution, store at -20°C and use within 1 month to prevent loss of potency. Aliquot to avoid multiple freeze/thaw cycles.

Research References

  1. [1] Barta A, Cebova M, Kovac A, et al. Aliskiren-Loaded Nanoparticles Downregulate (Pro)renin Receptor and ACE Gene Expression in the Heart of Spontaneously Hypertensive Rats: Effect on NADPH Oxidase. Int J Mol Sci (2024). PMID: 38255922 DOI: 10.3390/ijms25020846 Source material
  2. [2] Mahfoz AM, Gawish AY. Insight into the hepatoprotective, hypolipidemic, and antidiabetic impacts of aliskiren in streptozotocin-induced diabetic liver disease in mice. Diabetol Metab Syndr (2022). PMID: 36316746 DOI: 10.1186/s13098-022-00935-5 Source material
  3. [3] Zhi H, Luptak I, Alreja G, et al. Effects of direct Renin inhibition on myocardial fibrosis and cardiac fibroblast function. PLoS One (2013). PMID: 24349097 DOI: 10.1371/journal.pone.0081612 Source material

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