Evidence map›Paper›PMID 40985933›Full record

ReviewPhytotherapy research : PTR2025

Catalpol: An Iridoid Glycoside With Potential in Combating Cancer Development and Progression-A Comprehensive Review.

Lucas Fornari Laurindo, Victória Dogani Rodrigues, Elen Landgraf Guiguer, Lívia Fornari Laurindo, Debora Aparecida Pires de Campos Zuccari, Claudia Rucco Penteado Detregiachi, Adriano Cressoni Araújo, Jéssica da Silva Camarinha Oliveira, Durvanei Augusto Maria, Jefferson Aparecido Dias and 4 more

Abstract readReview
In one paragraph

Review in Phytotherapy research : PTR, 2025. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 5 papers.

0numbers the graph read from it
0cells of the map it votes in
5citing papers in PubMed
–field-weighted citation impact
1 · What the graph read from it

What it found

Each row is one number read from the abstract, on the scale the paper reported it, with its interval. Left of the dashed line favours the treatment, right favours the comparator. Under each row is the sentence it came from. New to these charts? A ten-minute tutorial.

The abstract states no effect estimate the extractor could read, or names no intervention and outcome on the map, so this paper lights no cell and moves no belief. It is still indexed, cited and linked below.

2 · The registry

The trial behind it

Trials whose registry record cites this paper, or whose number appears in the abstract. A trial that started after this paper was published is citing it as background, not reporting it.

Neither the registry nor the abstract names a trial number. If this is a trial report, that itself is worth knowing.

3 · Its place in the literature

Who cites it

5 citing papers in PubMed.

  1. Review
  2. Review
  3. Review
  4. Review
  5. Review
4 · The record

Corrections and comments

PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.

5 · Who and what money

Authors and funding

14 authors.

Lucas Fornari LaurindoDepartment of Biochemistry and Pharmacology, School of Medicine, Universidade de Marília (UNIMAR), Marília, São Paulo, Brazil.
Victória Dogani RodriguesDepartment of Biochemistry and Pharmacology, School of Medicine, Faculdade de Medicina de Marília (FAMEMA), Marília, São Paulo, Brazil.
Elen Landgraf GuiguerDepartment of Biochemistry and Pharmacology, School of Medicine, Universidade de Marília (UNIMAR), Marília, São Paulo, Brazil.
Lívia Fornari LaurindoDepartment of Molecular Biology, School of Medicine, Faculdade de Medicina de São José do Rio Preto (FAMERP), São José do Rio Preto, São Paulo, Brazil.
Debora Aparecida Pires de Campos ZuccariDepartment of Molecular Biology, School of Medicine, Faculdade de Medicina de São José do Rio Preto (FAMERP), São José do Rio Preto, São Paulo, Brazil.
Claudia Rucco Penteado DetregiachiPostgraduate Program in Structural and Functional Interactions in Rehabilitation, School of Medicine, Universidade de Marília (UNIMAR), Marília, São Paulo, Brazil.
Adriano Cressoni AraújoDepartment of Biochemistry and Pharmacology, School of Medicine, Universidade de Marília (UNIMAR), Marília, São Paulo, Brazil.
Jéssica da Silva Camarinha OliveiraDepartment of Biochemistry and Pharmacology, School of Medicine, Faculdade de Medicina de Marília (FAMEMA), Marília, São Paulo, Brazil.
Durvanei Augusto MariaDevelopment and Innovation Laboratory, Butantan Institute, São Paulo, São Paulo, Brazil.
Jefferson Aparecido DiasPostgraduate Program in Structural and Functional Interactions in Rehabilitation, School of Medicine, Universidade de Marília (UNIMAR), Marília, São Paulo, Brazil.
Rose Eli Grassi RiciPostgraduate Program in Structural and Functional Interactions in Rehabilitation, School of Medicine, Universidade de Marília (UNIMAR), Marília, São Paulo, Brazil.
Caroline Barbalho LamasDepartment of Gerontology, School of Gerontology, Universidade Federal de São Carlos (UFSCar), São Carlos, São Paulo, Brazil.
Rosa DireitoLaboratory of Systems Integration Pharmacology, Clinical and Regulatory Science, Research Institute for Medicines, Universidade de Lisboa (iMed.ULisboa), Lisboa, Portugal.
Sandra Maria BarbalhoDepartment of Biochemistry and Pharmacology, School of Medicine, Universidade de Marília (UNIMAR), Marília, São Paulo, Brazil.ORCID https://orcid.org/0000-0002-5035-876X

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Catalpol, a natural iridoid glycoside known for its anti-proliferative effects, has been proposed as an anticancer compound. Catalpol targets critical processes involved in cancer cell progression, like malignant proliferation, apoptosis, and metastasis. Additionally, catalpol presents potent anti-inflammatory and antioxidant properties crucial for cancer prevention and intervention. Due to the absence of clinical trials, this review investigates twelve studies, encompassing in vitro and animal trials from reputable databases, such as PubMed, with no time restrictions. Therefore, we covered evidence from catalpol's effects against several types of cancer, including breast, liver, colorectal, lung, gastric, bladder, and ovarian cancer, as well as osteosarcoma, and assessed various outcomes related to cell viability, apoptosis, migration, and modulation of molecular mechanisms by catalpol. Notably, catalpol induced cancer cell death via induction of mitochondrial apoptosis pathways, regulation of the expression of specific microRNAs, modulation of Sirt1, Kras, RACK1, PARP, PI3K/Akt, Bcl-2, and STAT3/JAK2/Src signaling pathways, and inactivation of NF-kB and Smad 2/3 signaling pathways. Furthermore, catalpol limits cancer metastasis due to modulation of critical metalloproteinases associated with cancer migration. Catalpol also synergizes with chemotherapeutic and adjuvant agents to induce cancer control, including regorafenib in liver cancer and chloroquine in gastric cancer, promoting increased anticancer action via upregulated cancer cell apoptosis, decreased proliferation, and inhibited angiogenesis via PI3K/p-Akt/mTOR/NF-κB, VEGF/VEGFR2, and Bax signaling pathways modulation. Catalpol derivatives also gained attention. Pyrazole-, imidazole-, and hydrolyzed-based catalpol derivatives increase cancer cell apoptosis and death and decrease tumor angiogenesis through similar pathways. This review seeks to provide understanding of catalpol's anticancer effects, its mechanisms of action, and its potential as a therapeutic anticancer agent while advocating for future research conductance.

Indexed as

Antineoplastic Agents, PhytogenicIridoid GlucosidesNeoplasmsAnimalsApoptosisCell MovementCell ProliferationDisease ProgressionHumansSignal TransductionAntineoplastic Agents, PhytogeniccatalpolIridoid Glucosidescancercatalpolinflammationmetastasisoxidative stressphytotherapy

Identifiers

PMID40985933
PMCPMC12504809

What Socratic holds

Textmetadata
LicenceCC BY
Read underepoch 390

Registered trials

None linked

Read under generation 80e0d062 · epoch 390. Bibliography from PubMed, PubMed Central and OpenAlex; grants from NIH RePORTER; trial links from ClinicalTrials.gov; estimates, votes and beliefs from the Socratic graph.