Aspartic Acid

Evidence Level: L5 Predicted Indications: 10

Table of Contents

  1. Aspartic Acid
  2. Aspartic Acid: From Potassium Deficiency to Renal Tubular Acidosis
    1. One-Sentence Summary
    2. Quick Overview
    3. Why is This Prediction Reasonable?
    4. Clinical Trial Evidence
    5. Literature Evidence
    6. Singapore Market Information
    7. Safety Considerations
    8. Conclusion and Next Steps
    9. Disclaimer

## Pharmacist Assessment Report

Aspartic Acid: From Potassium Deficiency to Renal Tubular Acidosis

One-Sentence Summary

Aspartic acid is a non-essential amino acid, originally used to treat potassium deficiency and widely present in parenteral nutrition solutions. The TxGNN model predicts it may be effective for renal tubular acidosis, but no clinical trials are registered and the 4 retrieved publications do not test aspartic acid as a treatment. This is a computational prediction with essentially no supporting clinical evidence.

Quick Overview

Item Content
Original Indication Potassium deficiency disease
Predicted New Indication Renal tubular acidosis
TxGNN Prediction Score 99.47%
Evidence Level L5
Singapore Market Status ✓ Marketed
Number of Registrations 7
Recommended Decision Hold

Why is This Prediction Reasonable?

Detailed mechanism of action data is not available. Based on known information, aspartic acid is an amino acid involved in the urea cycle and in renal ammonia and glutamine metabolism, which is loosely related to renal acid-base handling. It has been used in potassium-related supplementation, and mechanistically this could be tenuously linked to electrolyte and acid-base disorders.

However, the link is weak. None of the retrieved papers tests aspartic acid as a therapy for renal tubular acidosis. They cover genetic diagnosis of distal RTA, SLC4A1 mutations, a pyruvate carboxylase deficiency case with RTA, and tubular ammonia production. Standard RTA treatment is alkali replacement (bicarbonate or citrate), and there is no rationale for aspartate replacing it. The high TxGNN score should be read as a model output, not as clinical support.

Clinical Trial Evidence

Currently no related clinical trials registered.

Literature Evidence

PMID Year Type Journal Key Findings
6422151 1983 Case report J Inherit Metab Dis Neonate with pyruvate carboxylase deficiency, proximal RTA and cystinuria; the child began to thrive when the diet was supplemented with aspartic acid, asparagine and related amino acids (single case, confounded by the underlying metabolic disease)
26208211 2015 Genetic study J Pediatr (Rio J) Whole-exome sequencing for genetic diagnosis of distal RTA in four children
20068363 2010 Genetic study Nephron Physiol Distal RTA in Filipino children caused by SLC4A1 (AE1/Band 3) mutations
14301365 1965 Basic physiology Am J Physiol Relationship of tubular cell pNH3 to renal ammonia production

Literature for the other predicted indications (esophageal varices, dyspepsia, renal hypomagnesemia, hypophosphatemia, varicose disease, HELIX syndrome, Pendred syndrome, Alström syndrome) was also reviewed. It consists of unrelated genetic, structural or basic-science papers, or nothing at all, and none supports a therapeutic role for aspartic acid.

Singapore Market Information

Authorization Number Product Name Dosage Form Approved Indication
SIN08352P Aminoplasmal-15% Infusion Injection Not specified
SIN07846P Trophamine Injection 10% Injection Not specified
SIN07428P Vaminolact Intravenous Solution Injection Not specified
SIN15411P Aminoplasmal B.Braun 10% E Solution for Infusion Infusion, solution Not specified
SIN16734P Nutriflex Omega Special B. Braun Emulsion for Infusion Injection, emulsion Not specified

Two further registrations (SIN15469P, SIN15468P) are Nutriflex Omega products. All 7 registrations are valid single-ingredient entries, all injectable or infusion forms.

Safety Considerations

  • Disease associations flagged as contraindications in the knowledge graph (not label text): kidney disease, pyoureter, diarrheal disease, chronic diarrheal disease, atrioventricular block, hyperkalemic periodic paralysis, periodic paralysis, hypoaldosteronism, myotonia congenita, gastroparesis.

Kidney disease is notable given that the predicted indication is itself a renal disorder. Please refer to the package insert for further safety information.

Conclusion and Next Steps

Decision: Hold

Rationale: The prediction rests solely on a model score. There are no clinical trials, and the literature is either unrelated or a single confounded case report. Standard RTA therapy (alkali replacement) is well established, and there is no mechanistic reason for aspartate to substitute for it. The knowledge-graph contraindication with kidney disease adds further caution.

To proceed, the following is needed:

  • Package insert warnings and contraindications for the registered Singapore products (currently missing and blocking for safety screening)
  • Detailed mechanism of action data
  • Preclinical or clinical evidence that aspartic acid affects acid-base handling in RTA
  • Clarification of the approved indication text for the Singapore licences

    Disclaimer

This content is for research purposes only and does not constitute medical advice. Clinical validation is required before any clinical application.



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