Andrographolide (Andrographis paniculata)

Michael-acceptor diterpenoid that suppresses NF-κB/STAT3/HIF-1α and PI3K/Akt/mTOR, promotes apoptosis, and reduces angiogenesis/invasion; oral PK limits stand-alone use—best as chemo-sensitizer/adjunct.

← All agents

Human-reviewed · How we review →

AI extractedhuman reviewedsources checkedretractions suppressed

👥⭐⭐ Low to Moderate — Robust mechanistic and preclinical data (NF-κB/STAT3/HIF-1α, PI3K/Akt/mTOR, anti-angiogenesis/invasion); limited human oncology data and constrained oral bioavailability.Andrographis paniculata extractAndrographisAndro

Forms: Standardized A. paniculata extract (e.g., 10–30% andrographolide) · Purified andrographolide (research-grade/clinical-formulation dependent)

Educational only, not medical advice. OncoForge makes no claim that Andrographolide (Andrographis paniculata) treats, prevents, or cures any condition, beyond what the linked studies show. Evidence levels vary; effects may not translate to people, and some compounds can cause harm. Always coordinate with your oncology team.

Simple Summary

Andrographolide turns down master survival switches (NF-κB, STAT3) and hypoxia signaling (HIF-1α/VEGF), pushes cancer cells toward apoptosis, slows the cell cycle, and often blocks PI3K/Akt/mTOR. It also cuts invasion programs like MMP-2/9 and CXCR4. Because oral levels are low and short-lived in people, it’s best viewed as a chemo-sensitizer/adjunct rather than a stand-alone anticancer drug right now.

Evidence at a glance

Tier 2 · animalBreastLungEsophagealVarious (preclinical)

Strong mechanistic and animal data; limited human oncology evidence and low oral exposure.

How it may work

Andrographolide is a diterpenoid lactone that acts as a Michael acceptor. It directly and covalently modifies NF-κB p50 at Cys62 to block NF-κB DNA binding, suppressing transcription of survival, inflammatory, and pro-metastatic genes (e.g., COX-2, MMP-9). It inhibits JAK/STAT3 signaling (sensitizing cells to doxorubicin and other cytotoxics), downregulates HIF-1α (via PI3K/Akt suppression and ubiquitin-mediated degradation) and thereby lowers VEGF and angiogenesis. Across tumor models it induces mitochondrial apoptosis (caspase-3/7 activation, PARP cleavage, Bax↑/Bcl-2↓), triggers G0/G1 or G2/M arrest, and modulates autophagy in a context-dependent way (most often via PI3K/Akt/mTOR inhibition). It also reduces migration/invasion by lowering MMP-2/9, CXCR4, HER2 and related programs. PK in humans shows low oral bioavailability and short half-life; most clinical data are non-oncology, so anticancer efficacy in humans remains unproven.

Targets & pathways

Curated mechanistic targets reported for this agent — how it may act on cells, not proof of a clinical effect.

NF-κB↓Covalent p50 Cys62 → DNA binding ↓
STAT3↓
HIF-1α↓
PI3K/Akt/mTOR↓
COX-2↓
MMP-2↓
MMP-9↓
VEGF↓
Apoptosis↑
Cell cycle progression↓
Autophagy↕Context-dependent (often via PI3K/Akt/mTOR)
ROS↑
Invasion/Metastasis↓
Angiogenesis↓

NF-κB ↓STAT3 ↓HIF-1α ↓VEGF ↓MMP-2/9 ↓PI3K/Akt/mTOR ↓COX-2 ↓Apoptosis ↑Autophagy ↕ROS ↑Invasion/Metastasis ↓Angiogenesis ↓

Often studied / combined with

Combinations reported in the literature, not a protocol or a recommendation.

Doxorubicin, Cisplatin: NF-κB/STAT3/PI3K pathway suppression may enhance cytotoxic efficacy.
Curcumin: Convergent NF-κB/STAT3/HIF-1α modulation.

Overlapping mechanisms

NF-κB ↓, STAT3 ↓, PI3K/Akt/mTOR ↓: Avoid stacking multiple strong inhibitors of the same axes unless intentional with monitoring.

Safety & interactions

Severity and how well-established each signal is are shown separately. Verify everything with your oncologist or pharmacist — absence here does not mean safe.

Risk categories

Diarrhea RiskHypersensitivity RiskHypotension Risk MildPregnancy Avoid

Potential interactions

chemotherapy (general)MonitorMinorTheoreticalPathway inhibition (NF-κB/STAT3) may sensitize to cytotoxics; coordinate timing.
antihypertensivesDose AdjustMinorTheoreticalPotential additive BP-lowering effects.

Timing

With-meal: Improves GI tolerance.
AM
PM

References

Research

No published studies for Andrographolide (Andrographis paniculata) yet

New studies appear here once they’ve been reviewed. Browse all studies.

Dose: as studied, not a recommendation

These are doses as studied or reported, never a recommendation. The right amount of Andrographolide (Andrographis paniculata) depends on you, your other medicines, and your situation; decide it with your oncology team and pharmacist, not from a web page.

Ranges seen in adjunct / practice use: 300–600 mg (oral) Standardized A. paniculata extract per day (typically 30–50% andrographolide), divided BID–TID. ≈150–300 mg/day andrographolide-equivalent (AND-eq). Up to 900 mg extract (≈450 mg AND-eq) has been used in trials with medical oversight., Oral bioavailability is limited; divide doses for exposure. Match labels by % andrographolide (AND-eq). Consider clinician oversight above ~300 mg AND-eq/day..

Trials studying Andrographolide (Andrographis paniculata)

No actively-recruiting trials matched right now. Recruiting is not the same as proven. Search ClinicalTrials.gov →

Inclusion here is not an endorsement. OncoForge makes no claim beyond what the linked studies show. Discuss anything on this page with your oncology team before acting on it.

← All agents · Research Radar