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MEDICINAL PLANT & BOTANICAL REFERENCE PROFILE CODE: [BOT-14] ID: TIP-MED-000593

Yashtimadhu / Mulethi / Liquorice (Glycyrrhiza glabra)

Active Ingredient / Scientific Identity: Glycyrrhiza glabra L. • Class: Pharmacognosy & Phytochemistry • Fabaceae (Dried Peeled or Unpeeled Stolon and Root)

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1. Clinical & Scientific Overview

Yashtimadhu / Mulethi / Liquorice (Glycyrrhiza glabra) (TIP-MED-000593, Reference Code [BOT-14]) is classified under Medicinal Plants, Botanicals & Phytopharmaceuticals as a Pharmacognosy & Phytochemistry • Fabaceae (Dried Peeled or Unpeeled Stolon and Root). Within the Indian regulatory and compendial framework, it is governed under Indian Pharmacopoeia (IP) Monograph and API Part I Vol I; contraindicated in hypertension, heart failure, hypokalaemia, CKD, and pregnancy..

Verified Indian Market Examples / Compendial Status:
Standardised Pharmacopoeial Crude Drug / Extract (IP / API Reference)
Botanical Standardisation Note: Authenticate by macroscopic, microscopic, and HPTLC/HPLC marker assay (Triterpenoid saponin Glycyrrhizin (Glycyrrhizic acid — IP marker >=3.0% w/w, hydrolysed in gut to 18-beta-glycyrrhetinic acid) and prenylated flavonoids (Glabridin, Isoliquiritigenin)) per Indian Pharmacopoeia (IP) and Ayurvedic Pharmacopoeia of India (API).
Dosage Forms & Available Strengths:
Official Plant Part: Dried Peeled or Unpeeled Stolon and Root | Marker Compounds: Triterpenoid saponin Glycyrrhizin (Glycyrrhizic acid — IP marker >=3.0% w/w, hydrolysed in gut to 18-beta-glycyrrhetinic acid) and prenylated flavonoids (Glabridin, Isoliquiritigenin)
Routes: Oral / Topical as specified by classical API or standardized extract monograph

Pharmacognosy, Phytochemistry & Botanical Standardisation

Accepted Botanical Binomial & Authority: Glycyrrhiza glabra L.

Botanical Family: Fabaceae

Official Authenticated Plant Part: Dried Peeled or Unpeeled Stolon and Root

Major Phytochemical Constituents & IP/API Marker Compounds: Triterpenoid saponin Glycyrrhizin (Glycyrrhizic acid — IP marker >=3.0% w/w, hydrolysed in gut to 18-beta-glycyrrhetinic acid) and prenylated flavonoids (Glabridin, Isoliquiritigenin)

Yashtimadhu / Mulethi / Liquorice (Glycyrrhiza glabra) Botanical Reference Illustration

Traditional / Classical Ayurvedic Context: Traditional Kanthya (throat demulcent), Kasahara (expectorant), and gastric mucosal soothing root.

Modern Clinical Evidence Assessment (Clearly Distinguished from Traditional Use): Demulcent throat lozenges soothe acute pharyngitis; deglycyrrhizinated liquorice (DGL) supports gastric mucin secretion without mineralocorticoid toxicity.

Quality Control, Adulteration & Contaminant Limits: Authenticate via HPTLC/HPLC marker assay; screen for heavy metals (Lead <=10 ppm, Arsenic <=3 ppm, Cadmium <=0.3 ppm, Mercury <=1 ppm), microbial load, and aflatoxins B1/B2/G1/G2 per IP/API.

Indian Regulatory Classification (ASU vs Phytopharmaceutical vs FSSAI): Indian Pharmacopoeia (IP) Monograph and API Part I Vol I; contraindicated in hypertension, heart failure, hypokalaemia, CKD, and pregnancy.

3. Mechanism of Action & Pharmacodynamics

Major Phytochemical Constituents & Pharmacological Actions: Triterpenoid saponin Glycyrrhizin (Glycyrrhizic acid — IP marker >=3.0% w/w, hydrolysed in gut to 18-beta-glycyrrhetinic acid) and prenylated flavonoids (Glabridin, Isoliquiritigenin). Demulcent throat lozenges soothe acute pharyngitis; deglycyrrhizinated liquorice (DGL) supports gastric mucin secretion without mineralocorticoid toxicity.

4. Therapeutic Indications & Evidence-Supported Uses

  • Traditional / Classical Context: Traditional Kanthya (throat demulcent), Kasahara (expectorant), and gastric mucosal soothing root.
  • Modern Clinical Evidence Assessment: Demulcent throat lozenges soothe acute pharyngitis; deglycyrrhizinated liquorice (DGL) supports gastric mucin secretion without mineralocorticoid toxicity.

5. Educational Dosage Context, Formulations & Administration

Educational Dosing & Regimen Summary: Pharmacognostic & Clinical Evidence Summary: Demulcent throat lozenges soothe acute pharyngitis; deglycyrrhizinated liquorice (DGL) supports gastric mucin secretion without mineralocorticoid toxicity.

Administration & Meal Timing: Authenticated Plant Part Used: Dried Peeled or Unpeeled Stolon and Root. CLASSIC PSEUDOALDOSTERONISM MECHANISM: 18-beta-glycyrrhetinic acid potently inhibits renal 11-beta-hydroxysteroid dehydrogenase type 2 (11-beta-HSD2), preventing cortisol inactivation to cortisone in the distal nephron -> cortisol activates mineralocorticoid receptors -> severe hypertension, hypokalaemia, metabolic alkalosis, sodium/water retention, and suppressed plasma renin/aldosterone; precipitates digoxin toxicity and Torsades de Pointes via hypokalaemia!

6. Pharmacokinetics, Metabolism & Renal/Hepatic Adjustment

Absorption & Disposition:
Complex multicomponent phytoconstituent disposition involving intestinal deglycosylation by gut microbiota, hepatic Phase II glucuronidation/sulfation, and potential modulation of CYP450 and P-gp efflux pumps.
Metabolism & Biotransformation:
Intestinal microbial hydrolysis and hepatic Phase I/II biotransformation of secondary metabolites.
Elimination & Renal Adjustment:
Avoid unstandardised herbal extracts in Stage 3–5 Chronic Kidney Disease (risk of hyperkalaemia or nephrotoxic adulterants).
Hepatic Impairment Considerations:
Avoid high-dose concentrated botanical extracts in pre-existing hepatic disease; discontinue immediately if jaundice or transaminase elevation occurs.

7. Contraindications, Precautions & High-Risk Warnings

Contraindications & Red-Flag Precautions:
  • Hypersensitivity to Glycyrrhiza glabra L. or other members of the Fabaceae family
  • CLASSIC PSEUDOALDOSTERONISM MECHANISM: 18-beta-glycyrrhetinic acid potently inhibits renal 11-beta-hydroxysteroid dehydrogenase type 2 (11-beta-HSD2), preventing cortisol inactivation to cortisone in the distal nephron -> cortisol activates mineralocorticoid receptors -> severe hypertension, hypokalaemia, metabolic alkalosis, sodium/water retention, and suppressed plasma renin/aldosterone; precipitates digoxin toxicity and Torsades de Pointes via hypokalaemia!

Key Clinical Precautions: CLASSIC PSEUDOALDOSTERONISM MECHANISM: 18-beta-glycyrrhetinic acid potently inhibits renal 11-beta-hydroxysteroid dehydrogenase type 2 (11-beta-HSD2), preventing cortisol inactivation to cortisone in the distal nephron -> cortisol activates mineralocorticoid receptors -> severe hypertension, hypokalaemia, metabolic alkalosis, sodium/water retention, and suppressed plasma renin/aldosterone; precipitates digoxin toxicity and Torsades de Pointes via hypokalaemia!

8. Adverse Effects Profile

Common & Mechanism-Related Adverse Effects:
  • CLASSIC PSEUDOALDOSTERONISM MECHANISM: 18-beta-glycyrrhetinic acid potently inhibits renal 11-beta-hydroxysteroid dehydrogenase type 2 (11-beta-HSD2), preventing cortisol inactivation to cortisone in the distal nephron -> cortisol activates mineralocorticoid receptors -> severe hypertension, hypokalaemia, metabolic alkalosis, sodium/water retention, and suppressed plasma renin/aldosterone; precipitates digoxin toxicity and Torsades de Pointes via hypokalaemia!
Serious / Dose-Limiting Adverse Effects:
  • CLASSIC PSEUDOALDOSTERONISM MECHANISM: 18-beta-glycyrrhetinic acid potently inhibits renal 11-beta-hydroxysteroid dehydrogenase type 2 (11-beta-HSD2), preventing cortisol inactivation to cortisone in the distal nephron -> cortisol activates mineralocorticoid receptors -> severe hypertension, hypokalaemia, metabolic alkalosis, sodium/water retention, and suppressed plasma renin/aldosterone; precipitates digoxin toxicity and Torsades de Pointes via hypokalaemia!

9. Major Drug–Drug, Drug–Food & Drug–Herb Interactions

  • CLASSIC PSEUDOALDOSTERONISM MECHANISM: 18-beta-glycyrrhetinic acid potently inhibits renal 11-beta-hydroxysteroid dehydrogenase type 2 (11-beta-HSD2), preventing cortisol inactivation to cortisone in the distal nephron -> cortisol activates mineralocorticoid receptors -> severe hypertension, hypokalaemia, metabolic alkalosis, sodium/water retention, and suppressed plasma renin/aldosterone; precipitates digoxin toxicity and Torsades de Pointes via hypokalaemia!

10. Clinical Monitoring, Patient Counselling & Storage

Clinical & Laboratory Monitoring: Verify botanical binomial authenticity (exclude adulterants/substitutes), HPTLC marker content, heavy metal limits (Pb, As, Cd, Hg), aflatoxins, and pesticide residues per IP/API standards.

Pharmacist Patient Counselling Points:

  • Natural or herbal origin does NOT automatically mean risk-free; always disclose botanical supplements to your doctor and pharmacist.
  • CLASSIC PSEUDOALDOSTERONISM MECHANISM: 18-beta-glycyrrhetinic acid potently inhibits renal 11-beta-hydroxysteroid dehydrogenase type 2 (11-beta-HSD2), preventing cortisol inactivation to cortisone in the distal nephron -> cortisol activates mineralocorticoid receptors -> severe hypertension, hypokalaemia, metabolic alkalosis, sodium/water retention, and suppressed plasma renin/aldosterone; precipitates digoxin toxicity and Torsades de Pointes via hypokalaemia!
  • Never discontinue prescribed allopathic chronic disease medicines (antihypertensives, antidiabetics, anticonvulsants, or antivirals) in favour of unverified herbal products.

Storage, Stability & Dispensing Safeguards: Store dried botanical material and extracts in airtight, light-resistant containers below 25°C protected from humidity and fungal/aflatoxin contamination.

11. Visual Pharmacology & Mechanism Diagram (svg-v339-01-adme-12-step-journey)

THE 12-STEP ORAL DRUG JOURNEY THROUGH THE HUMAN BODY (LADME) Note: IV bolus enters Step 6 directly (F = 100%); Sublingual & Transdermal routes bypass Step 4–5 Portal First-Pass Metabolism 1. Oral Administration • Tablet / Capsule swallowed • Gastric emptying to duodenum pH 1.5–3.5 (Stomach) 2. Disintegration & Dissolution • Tablet breaks into granules • API dissolves in GI fluid Noyes-Whitney Dissolution Rate 3. GI Epithelial Absorption • Crosses intestinal villi • Passive / Active / P-gp efflux Small Intestine (Large Surface Area) 4. Portal Circulation • Mesenteric veins → Portal vein • Delivers blood to liver sinusoids Pre-systemic Venous Conduit 5. First-Pass Metabolism • Gut & hepatic CYP450 extraction • High: GTN, Propranolol, Morphine Determines Bioavailability (F = f_a × (1-E_H)) 6. Systemic Circulation • Hepatic vein → IVC → Heart • Unbound vs Albumin-bound drug Only FREE drug is active 7–8. Tissue Distribution (Vd) • Capillary permeation to organs • Blood-Brain & Placental barriers Vd = Dose / C_0 (L or L/kg) 9. Target Site of Action • Receptors (GPCR, Ion channel) • Enzymes & Carrier Transporters Pharmacodynamic Effect (E_max, EC50) 10. Hepatic Biotransformation • Phase I (CYP450 Oxidation/Hydrolysis) • Phase II (Glucuronidation/Sulfation) Converts lipophilic drug → hydrophilic metabolite 11. Renal & Biliary Elimination • Nephron: Filtration + Secretion − Reabsorption • Biliary excretion & Enterohepatic recycling Total Clearance CL_tot = CL_renal + CL_hepatic 12. Excretion from the Body • Urine (Primary polar metabolite route) • Bile/Faeces, Expired Air, Sweat, Milk Elimination Half-Life t1/2 = (0.693 × Vd) / CL
svg-v339-01-adme-12-step-journey — 8.1 Complete 12-Step Journey of an Orally Administered Drug (ADME): Figure 8.1: The 12-step physiological journey of a typical orally administered solid dosage form through Liberation, Absorption, Distribution, Metabolism, and Excretion (LADME). Note: Parenteral (IV), sublingual, and inhalational routes bypass gastrointestinal absorption and/or hepatic first-pass metabolism.

12. Authoritative References, Regulatory Sources & Editorial Disclaimer

Primary Compendial & Guideline Reference: Indian Pharmacopoeia (IP — Herbs and Herbal Products Addendum); Ayurvedic Pharmacopoeia of India (API — Ministry of AYUSH); CDSCO Rule 122E Phytopharmaceutical Drug Guidelines.

Official Verification Portals: Ministry of AYUSH — Pharmacopoeia Commission for Indian Medicine & Homoeopathy (PCIM&H) • Indian Pharmacopoeia Commission (IPC) — Herbal Monographs • CDSCO — Drugs and Cosmetics Rules (ASU & Phytopharmaceuticals)

Last Medically & Pharmaceutically Reviewed: 2026-11-10 • Verification Status: VERIFIED_EDUCATIONAL_CONTENT

Educational & Clinical Disclaimer: This reference profile is published solely for pharmacy education, academic study, and professional clinical reference. It does not substitute for patient-specific clinical judgement, qualified specialist oncology/medical supervision, or official CDSCO/IP prescribing information. Never self-medicate with prescription, Schedule H/H1/X, NDPS, or oncology medicines.