Biological Activity

Bioactivity / Mechanism

Diosgenin has been investigated in a 1,25D3-MARRS-associated neuronal pathway. It reduced cell-surface vitamin D3 ligand binding in rat cortical neurons, and an anti-MARRS antibody prevented its axonal-growth response in mouse cortical cultures. These assays support pathway involvement without establishing a purified-receptor affinity or an agonist EC50. [1,2]

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

Target & Activity

Target	Activity	Value
STAT3

Cellular Effect

Cell Line	Activity	Value	Description	Reference
A549	IC50	> 10 μM	Cytotoxicity against human A549 cells assessed as cell growth inhibition measured after 24 hrs by MTT assay	[PMID: 33381964]
A549	IC50	> 20 μM	Antiproliferative activity against human A549 cells assessed as reduction in cell viability incubated for 48 hrs by MTS assay	[PMID: 30822712]
A549	IC50	10.8 μM	Antiproliferative activity against human A549 cells assessed as reduction in cell viability after 48 hrs by MTT assay	[PMID: 31546197]
A549	IC50	26.41 μM	Cytotoxicity against human A549 cells assessed as reduction in cell viability measured after 48 hrs by MTT assay	[PMID: 31761382]
A549	IC50	32.85 μM	Cytotoxicity against human A549 cells assessed as inhibition of cell growth incubated for 48 hrs by CCK-8 assay	[PMID: 33740546]
ASPC1	IC50	63.11 μM	Antiproliferative activity against human ASPC1 cells assessed as inhibition of cell growth incubated for 48 hrs by CCK8 assay	[PMID: 35586422]
BXPC-3	GI50	1 μg/mL	Growth inhibition of humanBxPC3 cells after 48 hrs	[PMID: 15921418]
DU-145	GI50	8.5 μg/mL	Growth inhibition of human DU145 cells after 48 hrs	[PMID: 15921418]
GES1	IC50	100.7 μM	Cytotoxicity against human GES1 cells assessed as reduction in cell viability measured after 48 hrs by MTT assay	[PMID: 31761382]
HBL-100	IC50	10.8 μM	Antiproliferative activity against human HBL100 cells assessed as reduction in cell viability after 48 hrs by MTT assay	[PMID: 31546197]
HCT-116	IC50	10.8 μM	Antiproliferative activity against human HCT116 cells assessed as reduction in cell viability after 48 hrs by MTT assay	[PMID: 31546197]
HCT-116	IC50	31.41 μM	Antiproliferative activity against human HCT-116 cells assessed as inhibition of cell growth incubated for 48 hrs by CCK8 assay	[PMID: 35586422]
HCT-116	IC50	49.11 μM	Cytotoxicity against human HCT-116 cells assessed as reduction in cell viability measured after 48 hrs by MTT assay	[PMID: 31761382]
HeLa	IC50	> 50 μg/mL	Cytotoxicity against human HeLa cells after 6 days by SRB assay	[PMID: 22880631]
HepG2	IC50	> 10 μM	Cytotoxicity against human HepG2 cells assessed as cell growth inhibition measured after 24 hrs by MTT assay	[PMID: 33381964]
HepG2	IC50	> 50 μM	Cytotoxicity against human HepG2 cells after 48 hrs by MTT assay	[PMID: 23153797]
HepG2	IC50	33.87 μM	Cytotoxicity against human HepG2 cells assessed as reduction in cell viability measured after 48 hrs by MTT assay	[PMID: 31761382]
HepG2	IC50	48.36 μM	Cytotoxicity against human HepG2 cells assessed as inhibition of cell growth incubated for 48 hrs by CCK-8 assay	[PMID: 33740546]
HL-60	IC50	> 20 μM	Antiproliferative activity against human HL60 cells assessed as reduction in cell viability incubated for 48 hrs by MTS assay	[PMID: 30822712]
HT-29	IC50	> 50 μg/mL	Cytotoxicity against human HT-29 cells after 6 days by SRB assay	[PMID: 22880631]

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In Vitro Studies

In primary mouse cortical neurons, 1 μM diosgenin for four days increased axonal length per neuron under normal-IgG control conditions. Anti-1,25D3-MARRS pretreatment prevented this increase. The reported n = 21 refers to images per treatment. [2]

In PC-3 cells, diosgenin reduced collagen-filter invasion by a reported 22% at 10 μM and 40% at 20 μM after 24-hour pretreatment. These concentrations did not significantly reduce MTT viability at 24 or 48 hours; 30 μM was cytotoxic in that assay. The controls were reported as untreated, with ethanol exposure below 0.2%. [3]

Cell-surface vitamin D3 ligand displacement in cortical neurons

Cell-based study · Primary rat cortical neurons (Sprague-Dawley embryos; E17 specified in binding method) [1]

Diosgenin reduced the cell-surface immunoluminescence signal from 0.1 μM 1α,25-dihydroxyvitamin D3 (DHVD3). This is a cellular competition assay; it does not supply a purified-receptor affinity or diosgenin IC50.

Measured endpoints — not treatment concentrations
Endpoint	Reported result	Reference
Cell-surface DHVD3-associated luminescence relative to DHVD3 alone	Reported result Reduced with diosgenin at 0.1 and 10 μM; no exact displacement percentage extracted	[1]

Literature-Reported Treatment Conditions

Treatment concentration: Diosgenin 0.1 or 10 μM; DHVD3 0.1 μM
Exposure duration: 10 min
Method: Simultaneous ligand exposure; anti-DHVD3 immunoluminescence without membrane permeabilization
Vehicle: DMSO stocks reported; final solvent concentration for this binding assay not specified
Co-treatment: DHVD3 is the detected competing ligand, not a therapeutic combination
Reported limits: Replicate number and final solvent concentration are not specified for Fig. 3D; no fitted affinity reported.

Methods and source locations

Compound reported in the paper: Diosgenin; Compound label in the paper: Diosgenin

Compound-level literature evidence; not validation of an Adooq lot or a clinical-use claim.

Fig. 3D; Results cell-binding paragraph; Methods: Materials and Luminescence detection of 1,25D3-MARRS binding

Cell-surface DHVD3-associated luminescence relative to DHVD3 alone: Anti-DHVD3 immunoluminescence after 10-min exposure; DHVD3-alone comparator — Fig. 3D and Results cell-binding paragraph; Methods: Luminescence detection of 1,25D3-MARRS binding

Antibody-sensitive axonal growth in cortical neurons

Cell-based study · Primary mouse cortical neurons (ddY embryos, E14) [2]

Diosgenin increased pNF-H-positive axonal length per MAP2-positive neuron in normal-IgG cultures. The increase was absent after anti-1,25D3-MARRS antibody pretreatment, supporting involvement of this pathway in this neuronal model.

Measured endpoints — not treatment concentrations
Endpoint	Reported result	Reference
pNF-H-positive axon length per MAP2-positive neuron	Reported result Increase with diosgenin under normal IgG; no increase under anti-MARRS; *p < 0.05; n = 21 images per treatment	[2]

Literature-Reported Treatment Conditions

Treatment concentration: 1 μM diosgenin
Exposure duration: 4 days after diosgenin; antibody pretreatment for 15 min
Method: Axonal-length imaging; normal rabbit IgG or Ab099 at 1:500
Vehicle: Vehicle-treated cultures included; final culture-solvent composition not specified separately
Co-treatment: Ab099 or normal rabbit IgG used as mechanistic/control co-treatments
Reported limits: Twenty-one images per treatment were quantified; independent culture-preparation n is not reported. The in-vivo ethanol/glucose vehicle is not assigned to the culture assay.

Methods and source locations

Compound reported in the paper: Diosgenin; Compound label in the paper: Diosgenin

Compound-level literature evidence; not validation of an Adooq lot or a clinical-use claim.

Fig. 3; Results axonal-growth paragraph; Methods: Materials, Primary culture, Measurement of axonal density, Statistical analysis

pNF-H-positive axon length per MAP2-positive neuron: Immunocytochemistry and image analysis; mean with SE; two-tailed unpaired t-test reported — Fig. 3 and Methods: Measurement of axonal density

PC-3 invasion with a viability control

Cell-based study · Human prostate cancer PC-3 cells [3]

Diosgenin reduced PC-3 invasion through a type-I collagen-coated filter. The authors report 22% and 40% inhibition at 10 and 20 μM. MTT viability was not significantly reduced at 5–20 μM over 24 or 48 h, whereas 30 μM reduced viability; the invasion findings do not establish in-vivo metastasis inhibition.

Measured endpoints — not treatment concentrations
Endpoint	Reported result	Reference
Invasion inhibition relative to untreated control	Reported result 22% at 10 μM; 40% at 20 μM (reported in Results); three independent experiments; mean ± SD	[3]
MTT viability at invasion-relevant and higher concentrations	Reported result No significant reduction at 5–20 μM at 24 or 48 h; 30 μM significantly reduced viability (***p < 0.001); four independent experiments; mean ± SD	[3]

Literature-Reported Treatment Conditions

Treatment concentration: 5, 10 and 20 μM for invasion; 30 μM included only in the viability-control dose range
Exposure duration: 24-h pretreatment followed by 6-h invasion assay; MTT controls assessed at 24 and 48 h
Method: Type-I collagen-coated Boyden chamber; separate MTT viability assessment
Vehicle: Ethanol, final concentration <0.2%; comparisons reported against untreated controls
Co-treatment: Diosgenin alone
Reported limits: A separate solvent-matched control is not described; this is not a clinical or animal metastasis experiment.

Methods and source locations

Compound reported in the paper: Diosgenin; Compound label in the paper: Diosgenin

Compound-level literature evidence; not validation of an Adooq lot or a clinical-use claim.

Fig. 3A–B and Fig. 1; Results: Cytotoxic Effect and Diosgenin Inhibits Invasion; Methods: Reagents and Cell Culture, Cell Viability Assay, Boyden Chamber Invasion Assay, Statistical Analysis

Invasion inhibition relative to untreated control: Invaded cells counted in five random fields per treatment; one-way ANOVA with Dunnett test; Fig. 3 shows *p < 0.05 and **p < 0.01 — Fig. 3B; Results: Diosgenin Inhibits Invasion; Methods: Boyden Chamber Invasion Assay

MTT viability at invasion-relevant and higher concentrations: MTT assay; untreated comparator; no exact bar heights extracted — Fig. 1; Results: Cytotoxic Effect; Methods: Cell Viability Assay

In Vivo Studies

In female 5XFAD mice, diosgenin at 10 μmol/kg intraperitoneally once daily for 20 days improved object recognition and reduced selected brain pathology measures. The presynaptic effect was regional: swollen presynaptic area decreased in cortex but not hippocampus. Memantine reduced plaque burden without improving recognition under the tested regimen. [1]

In normal male mice, the training-to-test object-preference increase observed with diosgenin and aCSF was absent with anti-MARRS infusion. Cortical axonal-density responses were also attenuated by the antibody; hippocampal CA1 and CA3 showed no significant axonal-density increase. Small groups and the absence of an in-vivo isotype-antibody control limit the mechanistic inference. [2]

Recognition memory and brain histology in 5XFAD mice

Animal study · Female 5XFAD mice and non-transgenic littermates, 6–8 months old [1]

A 20-day diosgenin regimen improved object recognition in 5XFAD mice. Histology from the same experiment showed reduced plaque burden and swollen axonal area; the presynaptic effect was region-dependent. Memantine did not improve recognition under the tested regimen.

Measured endpoints — not treatment concentrations
Endpoint	Reported result	Reference
Novel-object preference	Reported result p < 0.05 versus vehicle-treated 5XFAD; n = 4–6 mice; mean with SE	[1]
Amyloid plaque area, PHF-tau immunoreactivity, swollen axons and swollen presynapses	Reported result Plaque and swollen-axon area reduced in cortex and hippocampus; PHF-tau reduction depended on plaque proximity; swollen-presynapse area reduced in cortex but not hippocampus	[1]
Behavioral and comparator limitations	Reported result Memantine did not improve recognition; it reduced plaque burden. No significant locomotor differences reported (data not shown)	[1]

Conditions shared by the study groups

Route: intraperitoneal
Frequency: once daily
Treatment course: 20 days
Vehicle: 10% DMSO in physiological saline

Study groups and reported outcomes
Group / dose	Comparator	Observed result	Reference
Diosgenin-treated 5XFAD 10 μmol/kg	Vehicle-treated 5XFAD and wild-type reference groups	Recognition preference improved; plaque and selected degeneration-associated histology measures decreased.	[1]
Vehicle-treated 5XFAD	Vehicle-treated 5XFAD and wild-type reference groups	Novel-object preference remained near chance; disease-model comparator.	[1]
Memantine comparator 200 μmol/kg memantine	Vehicle-treated 5XFAD and wild-type reference groups	No recognition-memory improvement under this regimen; amyloid plaque burden decreased.	[1]
Wild-type reference group	Vehicle-treated 5XFAD and wild-type reference groups	Novel-object preference above chance; no amyloid plaques observed.	[1]

Diosgenin-treated 5XFAD: Model: Female 5XFAD mice, 6–8 months; Reported limits: Per-group exact n is not provided in text; Fig. 1A reports n = 4–6 mice.

Vehicle-treated 5XFAD: Model: Female 5XFAD mice, 6–8 months; Reported limits: Per-group exact n is not provided in text; Fig. 1A reports n = 4–6 mice.

Memantine comparator: Model: Female 5XFAD mice, 6–8 months; Reported limits: Per-group exact n is not provided in text; Fig. 1A reports n = 4–6 mice.

Wild-type reference group: Model: Female non-transgenic littermates, 6–8 months; Reported limits: Per-group exact n is not provided in text; Fig. 1A reports n = 4–6 mice.

Methods and source locations

Compound reported in the paper: Diosgenin; Compound label in the paper: Diosgenin

Compound-level literature evidence; not validation of an Adooq lot or a clinical-use claim.

Figs. 1A–D and 2A–C; Methods: Animals, Novel object recognition test, Immunohistochemistry, Statistical analysis

Novel-object preference: Novel object recognition, 30-min interval; one-way ANOVA with Dunnett comparison; within-group training/test paired comparison also shown — Fig. 1A and Results opening paragraph; Methods: Novel object recognition test

Amyloid plaque area, PHF-tau immunoreactivity, swollen axons and swollen presynapses: Brain immunohistochemistry; area counts displayed in plots are sampled regions, not animal n. No numerical bar heights extracted — Figs. 1C–D and 2B–C; Results histology paragraphs; Methods: Immunohistochemistry

Behavioral and comparator limitations: Separate memantine arm; wild-type and 5XFAD vehicle controls; open-field result reported in text only — Fig. 1A,C; Results opening paragraph and plaque paragraph

Diosgenin-treated 5XFAD · Figs. 1A–D and 2A–C; Methods: Animals, Novel object recognition test, Immunohistochemistry, Statistical analysis

Vehicle-treated 5XFAD · Figs. 1A–D and 2A–C; Methods: Animals, Novel object recognition test, Immunohistochemistry, Statistical analysis

Memantine comparator · Figs. 1A–D and 2A–C; Methods: Animals, Novel object recognition test, Immunohistochemistry, Statistical analysis

Wild-type reference group · Figs. 1A–D and 2A–C; Methods: Animals, Novel object recognition test, Immunohistochemistry, Statistical analysis

Antibody-sensitive memory and regional axonal responses in normal mice

Animal study · Male ddY mice, 6 weeks old; vehicle/aCSF, diosgenin/aCSF and diosgenin/Ab099 groups [2]

With aCSF infusion, diosgenin-treated mice showed increased novel-object preference from training to testing; this increase was absent with anti-MARRS infusion. Axonal density increased in mPFC and perirhinal cortex, but not CA1 or CA3. Locomotor distance did not differ significantly.

Measured endpoints — not treatment concentrations
Endpoint	Reported result	Reference
Novel-object preference and open-field distance	Reported result Preference increase in aCSF/diosgenin group (*p < 0.05, paired training/test); absent in other shown groups; n = 4–6 mice. Locomotor distance: no significant group differences reported	[2]
Regional pNF-H-positive axonal density	Reported result Increased in mPFC and perirhinal cortex and attenuated by antibody; no significant increase in CA1 or CA3; *p < 0.05; n = 4–6 as captioned	[2]

Conditions shared by the study groups

Frequency: Diosgenin/vehicle once daily; infusion continuous
Treatment course: 6-day injection course; train day 5, test 48 h later
Vehicle: 10% ethanol in 5% glucose for systemic dosing; aCSF for infusion

Study groups and reported outcomes
Group / dose	Comparator	Observed result	Reference
aCSF plus vehicle	aCSF plus systemic vehicle	No training-to-test preference increase.	[2]
aCSF plus diosgenin 10 μmol/kg diosgenin	aCSF plus systemic vehicle	Training-to-test preference increased; axonal density increased in mPFC and perirhinal cortex.	[2]
Anti-MARRS plus diosgenin 10 μmol/kg diosgenin	aCSF plus systemic vehicle	No training-to-test preference increase; cortical axonal-density increases were attenuated.	[2]

aCSF plus vehicle: Model: Male ddY mice, 6 weeks old; Route: Diosgenin/vehicle intraperitoneal; aCSF infusion intracerebroventricular; Reported limits: No in-vivo isotype-antibody arm or antibody-only systemic-vehicle arm shown. Fig. 4 gives n = 4–6 mice.

aCSF plus diosgenin: Model: Male ddY mice, 6 weeks old; Route: Diosgenin/vehicle intraperitoneal; aCSF infusion intracerebroventricular; Reported limits: No in-vivo isotype-antibody arm or antibody-only systemic-vehicle arm shown. Fig. 4 gives n = 4–6 mice.

Anti-MARRS plus diosgenin: Model: Male ddY mice, 6 weeks old; Route: Diosgenin/vehicle intraperitoneal; Ab099 infusion in aCSF intracerebroventricular; Reported limits: No in-vivo isotype-antibody arm or antibody-only systemic-vehicle arm shown. Fig. 4 gives n = 4–6 mice.

Methods and source locations

Compound reported in the paper: Diosgenin; Compound label in the paper: Diosgenin

Compound-level literature evidence; not validation of an Adooq lot or a clinical-use claim.

Figs. 4–5; Results antibody-infusion and axonal-density paragraphs; Methods: Materials, Animals, Object recognition test, Immunohistochemistry, Surgical procedure, Statistical analysis

Novel-object preference and open-field distance: 48-h object-recognition test; mean with SE; two-tailed paired t-test; open-field distance over 10 min — Fig. 4A–B; Results antibody-infusion paragraph; Methods: Object recognition test

Regional pNF-H-positive axonal density: Axon length per 10,000 μm² tissue area; mean with SE; one-way ANOVA with Dunnett test. No bar-derived values extracted — Fig. 5A–E; Results axonal-density paragraph; Methods: Immunohistochemistry

aCSF plus vehicle · Figs. 4–5; Results antibody-infusion and axonal-density paragraphs; Methods: Materials, Animals, Object recognition test, Immunohistochemistry, Surgical procedure, Statistical analysis

aCSF plus diosgenin · Figs. 4–5; Results antibody-infusion and axonal-density paragraphs; Methods: Materials, Animals, Object recognition test, Immunohistochemistry, Surgical procedure, Statistical analysis

Anti-MARRS plus diosgenin · Figs. 4–5; Results antibody-infusion and axonal-density paragraphs; Methods: Materials, Animals, Object recognition test, Immunohistochemistry, Surgical procedure, Statistical analysis

Specifications

Manufacturer	Adooq Bioscience
Actions	Inhibitor
CAS Number	512-04-9
Applications	Pdia3/ERp57 activator, STAT3 inhibitor
Formula	C₂₇H₄₂O₃
Molecular Weight	414.6
SMILES	C[C@@]12[C@](C[C@@]3([H])[C@]2([H])[C@H](C)[C@]4(OC[C@H](C)CC4)O3)([H])[C@]5([H])CC=C6C[C@@H](O)CC[C@]6(C)[C@@]5([H])CC1

Storage & Solubility

In Vitro Solubility

Reported Solubility

Solvent	Reported Solubility
DMSO	Insoluble
Water	Insoluble
Ethanol	Warmed: 4 mg/mL (9.64 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] Tohda C, Urano T, Umezaki M, et al. Diosgenin is an exogenous activator of 1,25D₃-MARRS/Pdia3/ERp57 and improves Alzheimer's disease pathologies in 5XFAD mice Scientific reports (2012). PMID: 22837815 DOI: 10.1038/srep00535 Source material
[2] Tohda C, Lee YA, Goto Y, et al. Diosgenin-induced cognitive enhancement in normal mice is mediated by 1,25D₃-MARRS Scientific reports (2013). PMID: 24292207 DOI: 10.1038/srep03395 Source material
[3] Chen PS, Shih YW, Huang HC, et al. Diosgenin, a steroidal saponin, inhibits migration and invasion of human prostate cancer PC-3 cells by reducing matrix metalloproteinases expression PloS one (2011). PMID: 21629786 DOI: 10.1371/journal.pone.0020164 Source material

Publications

1 publication citing this product

Rashmi Rawat, .et al. , Food Chemistry Advances, 2022, 1: 100092

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Diosgenin

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Biological Activity

Bioactivity / Mechanism

Target & Activity

Cellular Effect

In Vitro Studies

Cell-surface vitamin D3 ligand displacement in cortical neurons

Literature-Reported Treatment Conditions

Antibody-sensitive axonal growth in cortical neurons

Literature-Reported Treatment Conditions

PC-3 invasion with a viability control

Literature-Reported Treatment Conditions

In Vivo Studies

Recognition memory and brain histology in 5XFAD mice

Conditions shared by the study groups

Antibody-sensitive memory and regional axonal responses in normal mice

Conditions shared by the study groups

Specifications

Storage & Solubility

In Vitro Solubility

Reported Solubility

Preparing Stock Solutions

Storage

Research References

Publications

Added to your cart

Documents & Downloads

Select a Size

Package Sizes

Diosgenin 50 mg

Free Aliquoting for Your Order

Biological Activity

Bioactivity / Mechanism

Target & Activity

Cellular Effect

In Vitro Studies

Cell-surface vitamin D3 ligand displacement in cortical neurons

Literature-Reported Treatment Conditions

Antibody-sensitive axonal growth in cortical neurons

Literature-Reported Treatment Conditions

PC-3 invasion with a viability control

Literature-Reported Treatment Conditions

In Vivo Studies

Recognition memory and brain histology in 5XFAD mice

Conditions shared by the study groups

Antibody-sensitive memory and regional axonal responses in normal mice

Conditions shared by the study groups

Specifications

Storage & Solubility

In Vitro Solubility

Reported Solubility

Preparing Stock Solutions

Storage

Research References

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