Art. -Nr.: HY-170409

BNN27

Name: BNN27
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SKU: HY-170409
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BNN27 is a blood-brain barrier-penetrant, selective NGF receptor (TrkA and p75NTR) activator. BNN27 activates ERK1/2/AKT. BNN27 enhances NGF-induced differentiation/axonal growth and inhibits JNK after NGF withdrawal. BNN27 reduces Amyloid-β plaques, gliosis, and pro-inflammatory cytokines, and rescues synaptic/cholinergic deficits, neurogenesis, and working memory. BNN27 can be used in research on Alzheimer's disease, amyotrophic lateral sclerosis, diabetic retinopathy, inflammatory hyperalgesia, anxiety disorders, and multiple sclerosis.

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Reinheit : 99.54%
CAS. Nr.: 1195795-81-3
Formel: C₂₁H₃₂O₃
Molecular Weight:332.48

Speicherung:

4°C, protect from light

* In solvent : -80°C, 6 months; -20°C, 1 month (protect from light)

BNN27 Chemical Structure

CAS. Nr.: 1195795-81-3

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Fluorescent Dye

Strong Fluorescence Signal / Multi-Disciplinary Applications / High Fluorescence Specificity

Biologische Aktivität
- Beschreibung
- IC₅₀ & Target
- In Vitro
- In Vivo
Chemical Information
Lösungsmittel & Löslichkeit
- In Vitro
- In Vivo
Reinheit & Dokumentation
Verweise
Help & FAQs
Classifications
Bioz

Biologische Aktivität

Beschreibung

IC₅₀ & Target

^[1]

TrkA

ERK1

ERK2

Alle Trk Receptor Isoform-spezifische Produkte anzeigen :

Alle ERK Isoform-spezifische Produkte anzeigen :

Alle Akt Isoform-spezifische Produkte anzeigen :

Alle JNK Isoform-spezifische Produkte anzeigen :

In Vitro

Aβ/Tau/α-Synuclein AggregationApoptosisOthers

Aβ/Tau/α-Synuclein Aggregation

BNN27 (100 nM) protects against Aβ42-induced cytotoxicity in P7 hippocampal NSCs through Trk and p75NTR receptors, but does not restore Aβ42-reduced BrdU (+)/Nestin (+) proliferation^[1].

Apoptosis

BNN27 (100 nM; 24 h) inhibits serum deprivation-induced apoptosis in PC12 cells in a TrkA-dependent manner^[3].

Others

BNN27 (10 μM; 2 h) is not a P-gp substrate in MDCK-MDR1 cells, with an efflux ratio of 3.7^[2].
BNN27 (18 h) shows high passive BBB permeability in the BBB-PAMPA assay, with a Pe of 12.7 μcm/s^[2].
BNN27 (10 μM; 2 h) is not a BCRP substrate in Caco-2 monolayer cells, with an efflux ratio of 1.5^[2].
BNN27 (1 pM-1 μM) effectively displaces [³H]-DHEA bound to membranes of HEK293^TrkA transfected cells (K_i = 1.8 nM)^[3].
Immobilized BNN27 (4°C overnight) directly pulls down recombinant TrkA^[3] in vitro.
BNN27 (100 nM; 15 min) activates TrkA by inducing phosphorylation of Y490, Y674/675, and Y785 in CHO^TrkA cells, but does not activate TrkB or TrkC^[3].
BNN27 (100 nM; 60 min) promotes TrkA localization to lipid raft microdomains in HEK293^TrkA cells^[3].

MedChemExpress (MCE) has not independently confirmed the accuracy of these methods. They are for reference only.

Western Blot Analysis^[3]

Cell Line:

CHO cells transfected with TrkA, TrkB, or TrkC cDNA
Concentration:

100 nM (BNN27)
Incubation Time:

15 min
Result:

Induced phosphorylation of TrkA at Y490, Y674/675, and Y785 in CHOTrkA transfectants.
However, BNN27 did not induce Y490 phosphorylation in CHO cells transfected with TrkB or TrkC cDNA.

Apoptosis Analysis^[3]

Cell Line:

PC12 cells transfected with shRNAs against TrkA
Concentration:

100 nM (BNN27)
Incubation Time:

24 h
Result:

FACS analysis of cells stained for cleaved Caspase-3 revealed that exposure to BNN27 reduced the number of apoptotic cells following serum deprivation from 34% (controls) to 15.33% (n=4).
Suppression of TrkA expression by shRNA almost completely reversed the anti-apoptotic effect of BNN27.

Western Blot Analysis^[3]

Cell Line:

HEK293 cells transfected with TrkA plasmid
Concentration:

100 nM (BNN27)
Incubation Time:

60 min
Result:

Exposure for 60 min to BNN27 caused the segregation of TrkA into lipid raft fractions identified by the presence of Flotillin-1.

In Vivo

Aβ/Tau/α-Synuclein AggregationApoptosisCarbohydrate MetabolismGlutamate Release or ReceptorsProtein/Amino Acid MetabolismInnate ImmunityCytokines & ChemokinesOxidative StressCytokines and ChemokinesOthers

Aβ/Tau/α-Synuclein Aggregation

BNN27 (10 mg/kg/day; subcutaneous injection; sustained release; 60 days) reduces hippocampal Aβ plaque burden, attenuates astrogliosis and microgliosis, rescues synaptic degeneration of CA2 mossy fibers, restores basal forebrain cholinergic soma size, reduces p75NTR⁺/ChAT⁺ neurons, promotes adult hippocampal neurogenesis, partially rescues dysregulated hippocampal proteins, and improves hippocampus-dependent spatial working memory in 5xFAD mice without altering TrkA⁺/ChAT⁺ neurons or entorhinal cortex neurofilament/myelin^[1].

Apoptosis

BNN27 (3 mg/day; intraperitoneal injection; daily; from gestational day 3 to E13.5) reduces apoptotic Caspase-3-positive sensory neurons in embryonic dorsal root ganglia of NGF-deficient mice^[3].
BNN27 (10 mg/kg; intraperitoneal injection; once every two days; 4 weeks) reverses diabetes-induced loss of bNOS/TH amacrine cell markers and reduces cleaved caspase-3, but does not reduce TUNEL⁺ retinal cell death in STZ diabetic rats^[6].

Carbohydrate Metabolism

BNN27 (19-470 mM; topical ophthalmic eye drops; daily; 7 days) restores diabetes-induced loss of NFL, bNOS, and TH immunoreactivity in the retina of diabetic Sprague-Dawley rats in a dose-dependent manner, with 94 and 470 mM being effective and 19 mM ineffective, and these effects are mediated by TrkA^R^[4].

Glutamate Release or Receptors

Protein/Amino Acid Metabolism

BNN27 (10-30 mg/kg; intraperitoneal injection; single injection; 30 minutes before sampling) produces dose- and sex-dependent changes in neurotransmitters and hormones, in which low doses increase hippocampal GABA, glutamine, and glutamate turnover as well as prefrontal glutamate in males, whereas 30 mg/kg alters testosterone and progesterone levels^[5].

Innate Immunity

Carbohydrate Metabolism

BNN27 (2-50 mg/kg; intraperitoneal injection; daily; 7 days) reverses diabetes-induced retinal neuronal/glial injury and inflammation in STZ diabetic rats through a TrkA-dependent mechanism, without reducing TUNEL⁺ retinal cell death^[6].

Innate Immunity

Cytokines & Chemokines

Oxidative Stress

BNN27 (100 mg/kg; intraperitoneal injection; once daily; for 4 consecutive days) reverses CFA-induced inflammatory hyperalgesia in mice^[7].

Innate Immunity

Cytokines and Chemokines

BNN27 (10-100 mg/kg; intraperitoneal injection; once daily; for 4 consecutive days) produces transient analgesia at 3 hours in CFA-induced inflammatory hyperalgesia in mice and reduces paw TNF-α without affecting edema^[7].

Innate Immunity

BNN27 (10-100 mg/kg; intraperitoneal injection; single dose 30 minutes before CFA) produces transient analgesia at 3 hours and reduces corticosterone in CFA-induced inflammatory hyperalgesia in mice^[7].
BNN27 (2.86 mg/day; subcutaneous implantation; 21-day release; implanted on day 8 and day 29) protects mature oligodendrocytes and myelin during Cuprizone-induced demyelination while reducing microgliosis and astrogliosis^[9].
BNN27 (2.86 mg/day; subcutaneous implantation; 21-day release; during 3-week remyelination after 6 weeks of Cuprizone treatment) does not improve remyelination after Cuprizone (HY-W115718) withdrawal, but reduces OPC number and glial cell activation^[9].

Others

BNN27 (90 mg/kg; intraperitoneal injection; single injection; 30 minutes before the open field test) suppresses locomotor and exploratory behavior in both sexes, whereas BNN27 (10-30 mg/kg; intraperitoneal injection; single injection; 30 minutes before each behavioral test) produces male-specific alterations in exploratory behavior in the open field, light-dark box, or hole board test, without anxiolytic-like effects^[5].
BNN27 (3-6 mg/kg; intraperitoneal injection; single injection 40 minutes before testing) increases the time spent in the light compartment of the light-dark box, indicating an anxiolytic-like effect in the light-dark box test^[8].

MedChemExpress (MCE) has not independently confirmed the accuracy of these methods. They are for reference only.

Animal Model:

C57Bl/6J background (male 5xFAD transgenic and age-matched male wild-type C57Bl/6J littermates; 1.5 months old at start; average weight ≈30 g)^[1]
Dosage:

10 mg/kg/day over 60 days (18 mg total; average animal weight ≈30 g)
Administration:

subcutaneous; continuous release; 60 days
Result:

Hippocampal Aβ-immunoreactive plaque load (6E10): 5xFAD mice receiving BNN27 had 13 plaques vs 5xFAD placebo mice with 23.78 plaques (n = 9).
Hippocampal GFAP-positive area: 5xFAD mice receiving BNN27 had 6.8585% vs 5xFAD placebo mice with 14.43% (n = 7-9).
Hippocampal IBA1-positive area: 5xFAD mice receiving BNN27 had 5.512% vs 5xFAD placebo mice with 11.75% (n = 7-9).
CA2 mossy fiber Synaptophysin-positive area: 5xFAD mice receiving BNN27 had 46.34% vs 5xFAD placebo mice with 16.68% (n = 6-9).
CA2 mossy fiber Synapsin I-positive signal: 5xFAD mice receiving BNN27 had 44.01% vs 5xFAD placebo mice with 21.79% (n = 6-9).
Basal forebrain ChAT+ soma size: 5xFAD mice showed reduced ChAT+ soma size vs WT (52.00 vs 67.9832); BNN27 administration restored the size of cholinergic neurons in 5xFAD mice.
Basal forebrain p75NTR+/ChAT+ neurons: number was increased in 5xFAD vs WT; BNN27 administration reduced the number of p75NTR+/ChAT+ neurons in 5xFAD mice compared with 5xFAD placebo.
Basal forebrain TrkA+/ChAT+ neurons: no change was observed in the number of TrkA+/ChAT+ neurons.
Entorhinal cortex neurofilament: BNN27 did not restore the genotype-observed reduction in neurofilament levels.
Entorhinal cortex myelin: no effect of BNN27 administration on the myelin condition.
T-maze spontaneous alternation performance: 5xFAD mice receiving BNN27 had 0.643 vs 5xFAD placebo mice with 0.4625.
Dentate gyrus BrdU+/NeuN+ neurons: 5xFAD mice receiving BNN27 had 858 vs 5xFAD placebo mice with 456.
Dentate gyrus DCX+ neurons: 5xFAD mice receiving BNN27 had 106.8 vs 5xFAD placebo mice with 82.2.
Proteomic rescue: BNN27 administration rescued 16 out of 47 down-regulated proteins by more than 10% and 38 out of 81 up-regulated proteins by more than 10%.
BNN27 administration rescued 54 out of 128 dys-regulated proteins.
In the 5xFAD+BNN27/WT comparison, 277 proteins were dys-regulated; 149 were regulated only in this comparison and 128 overlapped with the 5xFAD/WT comparison (5xFAD/WT comparison alone: 81 proteins dys-regulated).
The most rescued protein was Sptbn1; Ncstn showed minor rescue (−6%).

Animal Model:

C57BL/6 (ngf+/-; pregnant females; embryos at E13.5/E14)^[3]
Dosage:

3 mg/day
Administration:

i.p.; daily; gestation day 3 to E13.5
Result:

Significantly reduced the number of Caspase-3 positive neurons in the DRG to levels comparable to ngf+/+ embryos; reported as 31 vs 19 Caspase-3 positive neurons per section (n=6).

Animal Model:

Sprague-Dawley (adult female and male, 180-300 g)^[4]
Dosage:

19 mM; 94 mM; 470 mM
Administration:

topical ocular (eye drops); daily for 7 days beginning 4 weeks post-STZ
Result:

NFL-IR was 84.7% of mean gray area/section at 94 mM, 87.2% at 470 mM, and 62.5% at 19 mM (no effect).
bNOS-IR was 88.3% of cells/section at 94 mM, 93.0% at 470 mM, and 49.2% at 19 mM (no effect).
TH-IR was 91.6% of cells/section at 94 mM, 75.0% at 470 mM, and 25.0% at 19 mM (no effect).
TrkA phosphorylation: BNN27 94 mM produced a 1.8-fold increase in phospho/total TrkA ratio compared with non-treated diabetic retinas.
ERK1/2 phosphorylation: BNN27 94 mM produced 2.00 phospho/total ERK1/2 and approximately 2-fold increase compared with control retinas.
Co-administration of the specific TrkAR inhibitor (10^-3 M, intravitreal) reversed the BNN27-dependent effects at the optimum BNN27 dose of 94 mM on NFL-, bNOS-, and TH-IR compared with diabetic retinas treated with BNN27 alone; no statistically significant differences were observed in diabetic non-treated rat retinas in the presence or absence of the TrkAR inhibitor.

Animal Model:

Wistar (male and female; 3-month-old; outbred; non-husbanded; normally cycling females; group-housed 3-4 per cage)^[5]
Dosage:

10 mg/kg; 30 mg/kg; 90 mg/kg (open field test only)
Administration:

i.p.; single injection 30 min before each behavioral test; 90 mg/kg only before open field test
Result:

In the open field test, BNN27 90 mg/kg reduced horizontal distance travelled and vertical rearing counts in both sexes.
10 mg/kg and 30 mg/kg did not differ from vehicle.
In the light/dark box test, BNN27 30 mg/kg reduced the total number of transitions between the light and dark compartments.
Time spent in the illuminated compartment was not affected by BNN27.
In the hole-board test, BNN27 10 mg/kg and 30 mg/kg reduced the total number of holes explored in males only.
Both doses also increased the latency to explore the first hole and reduced the hole-board working memory index in males only.
No BNN27 effects were observed in female rats in the hole-board test.

Animal Model:

Wistar (male and female; 3-month-old; outbred; non-husbanded; normally cycling females; group-housed 3-4 per cage)^[5]
Dosage:

10 mg/kg; 30 mg/kg
Administration:

i.p.; three injections at 23, 5, and 1 h before forced swim test session
Result:

Did not affect immobility, swimming, or climbing duration during the forced swim test session.
Head-shake behavior was also not affected by BNN27.

Animal Model:

Wistar (male and female; 3-month-old; outbred; non-husbanded; normally cycling females; group-housed 3-4 per cage)^[5]
Dosage:

10 mg/kg; 30 mg/kg
Administration:

i.p.; single injection 30 min before decapitation and tissue/blood sampling
Result:

In the hippocampus, BNN27 10 mg/kg increased GABA and glutamine levels in both sexes.
Hippocampal glutamate levels were not affected by BNN27.
10 mg/kg increased the hippocampal glutamine/glutamate ratio, indicating increased glutamate turnover, in both sexes.
In the prefrontal cortex, BNN27 10 mg/kg increased glutamate levels in males only.
Prefrontal GABA, glutamine, and glutamate turnover were not affected by BNN27.
30 mg/kg decreased testosterone serum levels in males only, whereas BNN27 10 mg/kg did not.
30 mg/kg increased progesterone serum levels in both sexes; BNN27 10 mg/kg did not.
Did not affect estrogen serum levels.

Animal Model:

Sprague-Dawley (male and female, 180-300 g)^[6]
Dosage:

2 mg/kg i.p. daily for 7 days; 10 mg/kg i.p. daily for 7 days; 50 mg/kg i.p. daily for 7 days; 10 mg/kg i.p. daily for 7 days with intravitreal TrkAR inhibitor (10^-3 mol/L) on days 1, 4, and 6
Administration:

i.p.; daily for 7 days; intravitreal TrkAR inhibitor on days 1, 4, and 6
Result:

At 10 and 50 mg/kg reversed the diabetes-induced reduction in NFL-IR, bNOS-IR, and TH-IR; 2 mg/kg had no effect.
At 10 and 50 mg/kg increased TrkA Y490 phosphorylation to similar levels; 2 mg/kg had no effect.
Co-administered intravitreal TrkAR inhibitor reversed the BNN27 (10 mg/kg)-induced restoration of NFL-IR, bNOS-IR, and TH-IR compared with diabetic retinas treated with BNN27 alone.
Co-administered intravitreal TrkAR inhibitor reversed the BNN27 (10 mg/kg)-dependent increase in TrkA Y490 phosphorylation.
At 10 and 50 mg/kg attenuated the diabetes-induced increase in p75NTR-IR; 10 mg/kg reversed p75NTR expression.
Had no effect on the total number of TUNEL+ cells in the diabetic retina.
In retinas of diabetic rats treated with BNN27 (10 mg/kg), TUNEL+ cells and bNOS immunoreactivity were not colocalized.
Decreased cleaved caspase-3 immunoreactivity.
10 mg/kg: GFAP-IR 111.0% of mean gray area; 50 mg/kg: GFAP-IR 109.5%.
Diabetic retinas showed 149.0% and control retinas 100.0%.
10 mg/kg: Iba-1-positive cells 67 per mm2; 50 mg/kg: Iba-1-positive cells 113 per mm2.
Diabetic retinas showed 255 per mm2 and control retinas 100 per mm2.
10 mg/kg decreased TNFα and increased IL-10 and IL-4; 50 mg/kg reduced IL-1β.

Animal Model:

Sprague-Dawley (male and female, 180-300 g)^[6]
Dosage:

10 mg/kg i.p. every second day for 4 weeks
Administration:

i.p.; every second day; 4 weeks
Result:

Did not reduce the number of TUNEL+ cells per mm2 compared with the diabetic retina.
Reversed the diabetes-induced attenuation of bNOS and TH immunoreactive cells.
Decreased cleaved caspase-3 immunoreactivity.

Animal Model:

C57BL6x1291Sv (adult male, 8-12 weeks)^[7]
Dosage:

100 mg/kg
Administration:

i.p.; once daily; for 4 consecutive days
Result:

Reversed CFA-induced inflammatory hyperalgesia, with increased paw withdrawal latency at 3, 6, and 24 h following CFA.
At 6 h, increased leukocyte infiltration and MPO activity in the inflamed paw.
At 24 h, decreased immune cell infiltration and MPO activity compared with controls.
No effect on paw edema.
At 6 h, increased IL-6, TNF-α, and IL-10 levels in the inflamed paw and plasma.
At 24 h, decreased TNF-α in the inflamed paw and plasma.
IL-6 unchanged in the inflamed paw but decreased in plasma.
IL-10 remained elevated in the inflamed paw and plasma.
IL-1β in the inflamed paw showed no differences between groups at 24 h.
Plasma corticosterone was not different at 6 h, but was lower at 24 h.
Increased iNOS mRNA in the inflamed paw at 6 and 24 h.
Increased NGF mRNA in the inflamed paw at 6 h.
No change at 24 h.
At 6 h, total AKT2 unchanged, p-AKT2 and p-AKT2/total AKT2 ratio reduced.
At 24 h, total AKT2 and p-AKT2 increased, but p-AKT2/total AKT2 ratio unchanged.
No changes in AKT1.
Increased μ-opioid receptor mRNA at 6 h.
Increased POMC mRNA at 6 h and decreased POMC mRNA at 24 h.
Increased PENK mRNA at 24 h.
Decreased NGF mRNA in DRG at 6 and 24 h.
Decreased TrkA mRNA in the inflamed paw and DRG at 6 h.
At 24 h increased TrkA mRNA in DRG but no change in the inflamed paw.
No changes in p75NTR or substance P.
Increased serum β-endorphin.

Animal Model:

C57BL6x1291Sv (adult male, 8-12 weeks)^[7]
Dosage:

10 mg/kg
Administration:

i.p.; once daily; for 4 consecutive days
Result:

Affected paw withdrawal latency only at 3 h following the onset of inflammation.
No effect on leukocyte infiltration at 3 h.
Decreased inflamed paw TNF-α.
No effect on IL-6 and IL-10 in the inflamed paw or plasma.
Increased μ-opioid receptor, POMC, and PENK mRNA at 3 h.
Decreased NGF mRNA in DRG at 3 h.
No changes in TrkA mRNA in the inflamed paw or DRG at 3 h.

Animal Model:

C57BL6x1291Sv (adult male, 8-12 weeks)^[7]
Dosage:

100 mg/kg
Administration:

i.p.; single dose 30 min before CFA
Result:

Effective only 3 h following the onset of inflammation.
Did not alter leukocytic infiltration at 3 h.
Did not affect cytokine protein levels in the inflamed paw and plasma.
Decreased plasma corticosterone at 24 h.
Increased POMC mRNA at 3 h.
Decreased NGF mRNA in DRG at 3 h.
Increased TrkA mRNA in the inflamed paw and decreased TrkA mRNA in DRG.

Animal Model:

C57BL6x1291Sv (adult male, 8-12 weeks)^[7]
Dosage:

10 mg/kg
Administration:

i.p.; single dose 30 min before CFA
Result:

Had no effect on paw withdrawal latency.

Animal Model:

C57BL6x1291Sv (adult male, 8-12 weeks)^[7]
Dosage:

100 mg/kg and 10 mg/kg
Administration:

i.p.; single dose 30 min after CFA
Result:

Did not produce any effect on paw withdrawal latency for either dose.

Animal Model:

C57BL6x1291Sv (adult male, 8-12 weeks)^[7]
Dosage:

100 mg/kg (BNN27); 20 µL (10^-5 M) (TrkA inhibitor)
Administration:

i.p.; once daily; for 4 consecutive days (BNN27); intraplantar; once daily; for 4 consecutive days (TrkA inhibitor, simultaneously with BNN27)
Result:

Co-administration of BNN27 with TrkA inhibitor did not significantly alter paw withdrawal latency compared with controls at any time point tested.
Co-administration significantly decreased TNF-α and IL-10 at 24 h from the induction of inflammation, while IL-6 remained unchanged.
NGF mRNA levels in the inflamed paw were significantly elevated in mice co-receiving the TrkA inhibitor, whereas in DRG NGF mRNA levels remained significantly lower following TrkA inhibition.
No significant changes were observed in the mRNA levels of opioid peptide precursors and receptors after co-administration of BNN27 with the TrkA inhibitor.

Animal Model:

C57BL6x1291Sv (adult male, 8-12 weeks)^[7]
Dosage:

100 mg/kg (BNN27); 5 mg/kg (20 µL) (naloxone-HCl)
Administration:

i.p.; once daily; for 4 consecutive days (BNN27); intraplantar; single dose 30 min before CFA (naloxone-HCl)
Result:

Naloxone injection dramatically reduced paw withdrawal latency in mice receiving BNN27 compared with those receiving BNN27 only.
Co-administration of BNN27 and naloxone significantly reduced β-endorphin protein levels and PENK mRNA levels in the inflamed paw compared with mice receiving BNN27 only at 24 h from the onset of inflammation.

Animal Model:

Wistar (male, 3 months old, 250-300 g)^[8]
Dosage:

1 mg/kg, 3 mg/kg, and 6 mg/kg
Administration:

i.p.; single injection 40 min before testing
Result:

Administration of BNN27 did not affect the first entry into the dark chamber or the number of transitions between the two compartments.
Interestingly, BNN27 significantly increased the total time spent in the light chamber.
Vehicle-treated rats spent significantly less time in the lit chamber compared with rats treated with 3 or 6 mg/kg BNN27.
1 mg/kg did not increase time in the light chamber.\nTime spent in the central zone: BNN27 1 mg/kg, 9 s; BNN27 3 mg/kg, 14.5 s; BNN27 6 mg/kg, 14.3 s.
Number of squares crossed: BNN27 1 mg/kg, 98.4; BNN27 3 mg/kg, 94; BNN27 6 mg/kg, 99.
Number of rearings: BNN27 1 mg/kg, 32.5; BNN27 3 mg/kg, 35.6; BNN27 6 mg/kg, 35.3.
Grooming duration: BNN27 1 mg/kg, 6.8 s; BNN27 3 mg/kg, 7.3 s; BNN27 6 mg/kg, 4.9 s.
Did not affect the number of squares crossed or rearing episodes.
Appeared to reduce grooming duration, but this effect did not reach statistical significance.
Administration of BNN27 increased the time spent in the central zone of the apparatus.
Rats treated with 3 and 6 mg/kg BNN27 spent more time in the central zone of the OF apparatus compared with their vehicle-treated cohorts.

Animal Model:

Wistar (male, 3 months old, 250-300 g)^[8]
Dosage:

1 mg/kg, 3 mg/kg, and 6 mg/kg
Administration:

i.p.; single injection on day 3, 40 min before testing
Result:

Administration of BNN27 significantly reduced freezing duration.
Freezing levels of rats treated with 3 and 6 mg/kg BNN27 were significantly lower compared with those expressed by vehicle-treated animals.
1 mg/kg did not reduce freezing behavior.

Animal Model:

Wistar (male, 3 months old, 250-300 g)^[8]
Dosage:

3 mg/kg and 6 mg/kg; 5-HT2C receptor agonist 0.6 mg/kg
Administration:

i.p.; single injection 40 min before testing; 5-HT2C receptor agonist i.p. 10 min before testing
Result:

Grooming duration (median): vehicle + BNN27 3 mg/kg, 111.5 s; vehicle + BNN27 6 mg/kg, 104 s; 5-HT2C receptor agonist 0.6 mg/kg + BNN27 3 mg/kg, 174.5 s; 5-HT2C receptor agonist 0.6 mg/kg + BNN27 6 mg/kg, 189.5 s.
Rats receiving 5-HT2C receptor agonist plus vehicle displayed higher self-grooming compared with all other experimental groups including 5-HT2C receptor agonist + BNN27 3 mg/kg and 5-HT2C receptor agonist + BNN27 6 mg/kg.
Acute administration of BNN27 (3 and 6 mg/kg) attenuated excessive self-grooming caused by 5-HT2C receptor agonist.
Did not affect grooming activity in control animals.
Appeared to counteract the effects of 5-HT2C receptor agonist on horizontal (hypomotility) and vertical activity (decrease of rearings), but this action did not achieve statistical significance.

Animal Model:

C57B110/CBA (male, 8 weeks old)^[9]
Dosage:

2.86 mg/day; 60 mg total per pellet
Administration:

subcutaneous pellet; 21-day release; implanted at the beginning of the second week (Day 8) and the fifth week (Day 29) of cuprizone administration
Result:

BNN27 partially recovered cuprizone-induced decrease in MBP protein levels in the corpus callosum.
Significantly diminished myelin loss by Luxol Fast Blue staining.
MBP immunohistochemistry densitometric analysis showed that BNN27 reduced demyelination.
Partially but significantly counteracted the depletion of mature CC-1+ oligodendrocytes in the central and lateral corpus callosum after 6 weeks of cuprizone.
BNN27-treated mice showed milder PDGFRα+ OPC recruitment, with reduced OPC number compared with cuprizone alone.
BNN27 significantly decreased IBA-1+ microglia accumulation and GFAP+ astrocyte reactivity in the corpus callosum after 6 weeks of cuprizone.
At 3 and 5 weeks of cuprizone feeding, BNN27 reduced oligodendrocyte death, decreased OPC number, and decreased microglial and astrocytic activation.

Animal Model:

C57B110/CBA (male, 8 weeks old)^[9]
Dosage:

2.86 mg/day; 60 mg total per pellet
Administration:

subcutaneous pellet; 21-day release; implanted after 6 weeks of cuprizone administration during the 3-week remyelination period
Result:

No evident differences were present between the cuprizone and BNN27 groups in MBP densitometric analysis or oligodendrocyte number after 6 weeks of cuprizone followed by 3 weeks of remyelination.
In BNN27-treated mice, the OPC number was reduced compared with the cuprizone group.
Decreased microglia activation and astrogliosis.

Related Protocols :

Chemical Information

CAS. Nr. 1195795-81-3
Appearance Solid
Molecular Weight 332.48
Formel C₂₁H₃₂O₃
Color White to off-white
SMILES

C[C@@]12[C@]3(CC[C@@]1([H])[C@@]4([H])[C@]([C@@]5(C(C[C@H](CC5)O)=CC4)C)([H])CC2)[C@H](O3)CO
Versand

Room temperature in continental US; may vary elsewhere.
Speicherung

4°C, protect from light

* In solvent : -80°C, 6 months; -20°C, 1 month (protect from light)

Lösungsmittel & Löslichkeit

In Vitro:

DMSO : 100 mg/mL (300.77 mM; Need ultrasonic; Hygroscopic DMSO has a significant impact on the solubility of product, please use newly opened DMSO)

View the Complete Stock Solution Preparation Table

Preparing Stock Solutions

View the Complete Stock Solution Preparation Table

Concentration Solvent Mass

1 mg

5 mg

10 mg

Concentration

Solvent

Mass

1 mM

3.0077 mL

15.0385 mL

30.0770 mL

5 mM

0.6015 mL

3.0077 mL

6.0154 mL

10 mM

0.3008 mL

1.5038 mL

3.0077 mL

Please refer to the solubility information to select the appropriate solvent. Once prepared, please aliquot and store the solution to prevent product inactivation from repeated freeze-thaw cycles.

Storage method and period of stock solution: -80°C, 6 months; -20°C, 1 month (protect from light). When stored at -80°C, please use it within 6 months. When stored at -20°C, please use it within 1 month.

Molaritätsrechner

Mass (g) = Concentration (mol/L) × Volume (L) × Molecular Weight (g/mol)

Mass Mass

Konzentration Konzentration

Volumen Volumen

Molecular Weight Molecular Weight

Verdünnungsrechner

Konzentration _{(Stammlösung)} × Volumen _{(Stammlösung)} = Konzentration _{(Ziellösung)} × Volumen _{(Ziellösung)}

Konzentration _{(Stammlösung)} Konzentration _{(Stammlösung)}

Volumen _{(Stammlösung)} Volumen _{(Stammlösung)}

Konzentration _{(Ziellösung)} Konzentration _{(Ziellösung)}

Volumen _{(Ziellösung)} Volumen _{(Ziellösung)}

In Vivo:

Select the appropriate dissolution method based on your experimental animal and administration route.

Stock Solution Working Solution

For the following dissolution methods, please ensure to first prepare a clear stock solution using an In Vitro approach and then sequentially add co-solvents:
To ensure reliable experimental results, the clarified stock solution can be appropriately stored based on storage conditions. As for the working solution for In Vivo experiments, it is recommended to prepare freshly and use it on the same day.
The percentages shown for the solvents indicate their volumetric ratio in the final prepared solution. If precipitation or phase separation occurs during preparation, heat and/or sonication can be used to aid dissolution.

Protocol 1

Add each solvent one by one: 10% DMSO 40% PEG300 5% Tween-80 45% Saline

Solubility: 2.5 mg/mL (7.52 mM); Suspended solution; Need ultrasonic

This protocol yields a suspended solution of 2.5 mg/mL. Suspended solution can be used for oral and intraperitoneal injection.

Taking 1 mL working solution as an example, add 100 μL DMSO stock solution (25.0 mg/mL) to 400 μL PEG300, and mix evenly; then add 50 μL Tween-80 and mix evenly; then add 450 μL Saline to adjust the volume to 1 mL.

Protocol 2

Add each solvent one by one: 10% DMSO 90% (20% SBE-β-CD in Saline)

Solubility: 2.5 mg/mL (7.52 mM); Suspended solution; Need ultrasonic

This protocol yields a suspended solution of 2.5 mg/mL. Suspended solution can be used for oral and intraperitoneal injection.

Taking 1 mL working solution as an example, add 100 μL DMSO stock solution (25.0 mg/mL) to 900 μL 20% SBE-β-CD in Saline, and mix evenly.

Protocol 3

Add each solvent one by one: 10% DMSO 90% Corn Oil

Solubility: ≥ 2.5 mg/mL (7.52 mM); Clear solution

This protocol yields a clear solution of ≥ 2.5 mg/mL (saturation unknown). If the continuous dosing period exceeds half a month, please choose this protocol carefully.

Taking 1 mL working solution as an example, add 100 μL DMSO stock solution (25.0 mg/mL) to 900 μL Corn oil, and mix evenly.

In Vivo Dissolution Calculator

Please enter the basic information of animal experiments:

Dosage Dosage
mg/kg
Animal Weight (Per Animal) Animal Weight (Per Animal)
g
Dosing Volume (Per Animal) Dosing Volume (Per Animal)
μL
Number of Animals Number of Animals

Recommended: Prepare an additional quantity of animals to account for potential losses during experiments.

Recommended: Prepare an additional quantity of animals to account for potential losses during experiments.

Please enter your animal formula composition:

%
DMSO +

Recommended: Keep the proportion of DMSO in working solution below 2% if your animal is weak.
%
+
+
%
Tween-80 + +
%
Saline +

The co-solvents required include: DMSO, . All of co-solvents are available by MedChemExpress (MCE). , Tween 80. All of co-solvents are available by MedChemExpress (MCE).

Working solution concentration: 0.22 mg/mL

Reinheit & Dokumentation

Select Batch:

Reinheit: 99.98%

Assay: 99.98%

ee.: 99.98%

Data Sheet (333 KB)
SDS (252 KB)
- English - EN (252 KB)
- Français - FR (252 KB)
- Deutsch - DE (252 KB)
- Norwegian - NO (252 KB)
- Español - ES (252 KB)
- Swedish - SV (252 KB)
- Italian - IT (252 KB)
- Korean - KR (252 KB)
- Portuguese - PT (252 KB)
COA (2659 KB)
Elemental Analysis Report (2659 KB)
HNMR (2659 KB)
CNMR (2659 KB)
RP-HPLC (2659 KB)
NP-HPLC (2659 KB)
MS (2659 KB)
LCMS (2659 KB)
IR (2659 KB)
GC (2659 KB)
OR (2659 KB)
SDS-PAGE (2659 KB)
SEC-HPLC (2659 KB)
Other Report (2659 KB)
Handling Instructions (2659 KB)

Verweise

[1]. Kokkali M, et al. Multimodal beneficial effects of BNN27, a nerve growth factor synthetic mimetic, in the 5xFAD mouse model of Alzheimer’s disease. Molecular Psychiatry. 2025 Jun;30(6):2265-83.

[2]. Bennett JP, et al. Pharmacological properties of microneurotrophin drugs developed for treatment of amyotrophic lateral sclerosis. Biochemical pharmacology. 2016 Oct 01;117:68-77.

[3]. Pediaditakis I, et al. Selective and differential interactions of BNN27, a novel C17-spiroepoxy steroid derivative, with TrkA receptors, regulating neuronal survival and differentiation. Neuropharmacology. 2016 Dec;111:266-282.

[4]. Ibán-Arias R, et al. Effect of topical administration of the microneurotrophin BNN27 in the diabetic rat retina. Graefe's archive for clinical and experimental ophthalmology = Albrecht von Graefes Archiv fur klinische und experimentelle Ophthalmologie. 2019 Nov;257(11):2429-2436.

[5]. Kokras N, et al. Psychoactive properties of BNN27, a novel neurosteroid derivate, in male and female rats. Psychopharmacology. 2020 Aug;237(8):2435-2449. [Content Brief]

[6]. Ibán-Arias R, et al. The Synthetic Microneurotrophin BNN27 Affects Retinal Function in Rats With Streptozotocin-Induced Diabetes. Diabetes. 2018 Feb;67(2):321-333.

[7]. Poulaki S, et al. Analgesic and Anti-Inflammatory Effects of the Synthetic Neurosteroid Analogue BNN27 during CFA-Induced Hyperalgesia. Biomedicines. 2021 Sep 09;9(9):1185.

[8]. Fragkiadaki E, et al. Effects of low doses of the novel dehydroepiandrosterone (DHEA) derivative BNN27 in rat models of anxiety. Psychopharmacology. 2024 Feb;241(2):341-350.

[9]. Bonetto G, et al. The novel synthetic microneurotrophin BNN27 protects mature oligodendrocytes against cuprizone-induced death, through the NGF receptor TrkA. Glia. 2017 Aug;65(8):1376-1394.

Help & FAQs

How should lyophilized recombinant proteins be reconstituted and stored?

1. Before opening the cap, centrifuge the vial at 13000 rpm for 20-30 seconds. This step will ensure that any lyophilized powder that may have adhered to the cap or walls is collected at the bottom of the vial, minimizing the risk of product loss.

Complete Stock Solution Preparation Table

Optional Solvent	Concentration Solvent Mass	1 mg	5 mg	10 mg	25 mg
DMSO	1 mM	3.0077 mL	15.0385 mL	30.0770 mL	75.1925 mL
	5 mM	0.6015 mL	3.0077 mL	6.0154 mL	15.0385 mL
	10 mM	0.3008 mL	1.5038 mL	3.0077 mL	7.5192 mL
	15 mM	0.2005 mL	1.0026 mL	2.0051 mL	5.0128 mL
	20 mM	0.1504 mL	0.7519 mL	1.5038 mL	3.7596 mL
	25 mM	0.1203 mL	0.6015 mL	1.2031 mL	3.0077 mL
	30 mM	0.1003 mL	0.5013 mL	1.0026 mL	2.5064 mL
	40 mM	0.0752 mL	0.3760 mL	0.7519 mL	1.8798 mL
	50 mM	0.0602 mL	0.3008 mL	0.6015 mL	1.5038 mL
	60 mM	0.0501 mL	0.2506 mL	0.5013 mL	1.2532 mL
	80 mM	0.0376 mL	0.1880 mL	0.3760 mL	0.9399 mL
	100 mM	0.0301 mL	0.1504 mL	0.3008 mL	0.7519 mL

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BNN27

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