ProForma 2.0
validated simple linear
DVQPPGLKVWSDPFNH
Phoenixin-14 amide
Aliases: Phoenixin-14 amide
Normalized sequence
DVQPPGLKVWSDPFNH
16 amino acids
Release PepDiana-V1-20260620
26
Activity records
1
Source papers
11
Positive
15
Negative / threshold
Versioned scientific descriptors
No separate physicochemical property was reported in the primary-literature identity record. PepDiana release values are shown as computed properties.
Molecular weight
1836.011 Da
Molecular formula
C85H122N22O24
Theoretical pI
5.2109
Net charge at pH 7
-1.1515
GRAVY
-0.8125
Instability index
34.875
Aromaticity
0.125
Topological polar surface area
724.95 Ų
cLogP
-5.6775
Hydrogen-bond donors
22
Hydrogen-bond acceptors
24
Rotatable bonds
52
Method: PepDiana sequence/structure descriptor pipeline
Tool: Biopython+RDKit · Biopython 1.85; RDKit 2024.09.6
Calculated: 2026-06-20T11:01:38.358971+00:00
Assumptions: ph=7; termini=free N-terminus and free C-terminus for simple linear peptides; stereochemistry=standard L-amino acids; smiles_length_limit=200
ProForma 2.0
validated simple linear
DVQPPGLKVWSDPFNH
HELM 2.0
validated simple linear
PEPTIDE1{D.V.Q.P.P.G.L.K.V.W.S.D.P.F.N.H}$$$$V2.0
Canonical SMILES
validated
CC(C)CC(NC(=O)CNC(=O)C1CCCN1C(=O)C1CCCN1C(=O)C(CCC(N)=O)NC(=O)C(NC(=O)C(N)CC(=O)O)C(C)C)C(=O)NC(CCCCN)C(=O)NC(C(=O)NC(Cc1c[nH]c2ccccc12)C(=O)NC(CO)C(=O)NC(CC(=O)O)C(=O)N1CCCC1C(=O)NC(Cc1ccccc1)C(=O)NC(CC(N)=O)C(=O)NC(Cc1c[nH]cn1)C(=O)O)C(C)C
Isomeric SMILES
validated
CC(C)C[C@H](NC(=O)CNC(=O)[C@@H]1CCCN1C(=O)[C@@H]1CCCN1C(=O)[C@H](CCC(N)=O)NC(=O)[C@@H](NC(=O)[C@@H](N)CC(=O)O)C(C)C)C(=O)N[C@@H](CCCCN)C(=O)N[C@H](C(=O)N[C@@H](Cc1c[nH]c2ccccc12)C(=O)N[C@@H](CO)C(=O)N[C@@H](CC(=O)O)C(=O)N1CCC[C@H]1C(=O)N[C@@H](Cc1ccccc1)C(=O)N[C@@H](CC(N)=O)C(=O)N[C@@H](Cc1c[nH]cn1)C(=O)O)C(C)C
Paper-level observations
All PNX-14-treated groups exhibited a reduction in weight gain compared to PCOS (23 ± 2.1%, 21 ± 1.8%, and 20 ± 1.6%, respectively), with statistically significant differences observed in the 5 nmol group (P < 0.05).
All PNX-14-treated groups exhibited a reduction in weight gain compared to PCOS (23 ± 2.1%, 21 ± 1.8%, and 20 ± 1.6%, respectively), with statistically significant differences observed in the 5 nmol group (P < 0.05).
All PNX-14-treated groups exhibited a reduction in weight gain compared to PCOS (23 ± 2.1%, 21 ± 1.8%, and 20 ± 1.6%, respectively), with statistically significant differences observed in the 5 nmol group (P < 0.05).
Table 1: FSH (IU/L) PNX 2.5 group 7.54 ± 0.83. Text: While FSH levels showed a trend toward recovery in PNX-14-treated groups (ranging from 7.54 ± 0.83 to 9.24 ± 0.72 IU/L), these increases were not statistically significant.
Table 1: FSH (IU/L) PNX 5 group 7.93 ± 0.83. Text: While FSH levels showed a trend toward recovery in PNX-14-treated groups (ranging from 7.54 ± 0.83 to 9.24 ± 0.72 IU/L), these increases were not statistically significant.
Table 1: FSH (IU/L) PNX 30 group 9.24 ± 0.72. Text: While FSH levels showed a trend toward recovery in PNX-14-treated groups (ranging from 7.54 ± 0.83 to 9.24 ± 0.72 IU/L), these increases were not statistically significant.
Table 1: LH (mIU/mL) PNX 2.5 group 6.07 ± 1.07. Text: PNX-14 administration did not significantly alter LH levels in any dose group (P > 0.05).
Table 1: LH (mIU/mL) PNX 5 group 5.11 ± 0.83. Text: PNX-14 administration did not significantly alter LH levels in any dose group (P > 0.05).
Table 1: LH (mIU/mL) PNX 30 group 6.42 ± 0.71. Text: PNX-14 administration did not significantly alter LH levels in any dose group (P > 0.05).
Table 1: Testosterone (pg/mL) PNX 2.5 group 408.2 ± 49.25. Text: Serum testosterone concentrations were moderately elevated in the PCOS (402.1 ± 23.33 pg/mL) and PNX 2.5 nmol (408.2 ± 49.25 pg/mL) groups compared to the control group (353.5 ± 20.36 pg/mL), but these differences were not statistically significant.
Table 1: Testosterone (pg/mL) PNX 5 group 336.4 ± 38.15. Text: Testosterone levels declined at higher PNX doses (336.4 ± 38.15 and 345.4 ± 16.85 pg/mL for PNX 5 and 30 nmol, respectively), yet remained within the variability of the control group.
Table 1: Testosterone (pg/mL) PNX 30 group 345.4 ± 16.85. Text: Testosterone levels declined at higher PNX doses (336.4 ± 38.15 and 345.4 ± 16.85 pg/mL for PNX 5 and 30 nmol, respectively), yet remained within the variability of the control group.
Table 1: Progesterone (ng/mL) PNX 2.5 group 23.85 ± 1.8. Text: treatment with PNX-14 at all doses (23.85–25.57 ng/mL) failed to significantly restore progesterone levels, and values remained similar to those in the PCOS group.
Table 1: Progesterone (ng/mL) PNX 5 group 25.57 ± 0.68. Text: treatment with PNX-14 at all doses (23.85–25.57 ng/mL) failed to significantly restore progesterone levels, and values remained similar to those in the PCOS group.
Table 1: Progesterone (ng/mL) PNX 30 group 24.51 ± 0.84. Text: treatment with PNX-14 at all doses (23.85–25.57 ng/mL) failed to significantly restore progesterone levels, and values remained similar to those in the PCOS group.
Table 1: Estradiol (ng/L) PNX 2.5 group 54.58 ± 5.85. Text: While the lowest level was observed in the PNX 2.5 nmol group (54.58 ± 5.85 ng/L), higher PNX-14 doses (PNX 5: 74.67 ± 7.62; PNX 30: 71.43 ± 5.59 ng/L) did not significantly differ from the PCOS group, indicating no robust estradiol recovery with treatment.
Table 1: Estradiol (ng/L) PNX 5 group 74.67 ± 7.62. Text: higher PNX-14 doses (PNX 5: 74.67 ± 7.62; PNX 30: 71.43 ± 5.59 ng/L) did not significantly differ from the PCOS group, indicating no robust estradiol recovery with treatment.
Table 1: Estradiol (ng/L) PNX 30 group 71.43 ± 5.59. Text: higher PNX-14 doses (PNX 5: 74.67 ± 7.62; PNX 30: 71.43 ± 5.59 ng/L) did not significantly differ from the PCOS group, indicating no robust estradiol recovery with treatment.
PNX-14 treatment at 2.5 nmol significantly improved primordial follicle numbers (24.2 ± 2.8%; P < 0.05 vs PCOS), whereas higher doses showed no further improvement (Fig. 3A).
Treatment with PNX-14 at 2.5 nmol increased this count to 9.8 ± 1.0% (P < 0.05 vs PCOS), with no significant changes observed at higher doses (Fig. 3D).
Multilaminar-primary follicle counts were significantly elevated in PNX 5 (16.8 ± 1.9%) and PNX 30 (14.7 ± 2.2%) groups compared to both PCOS (9.4 ± 1.4%) and control groups (8.6 ± 1.1%) (P < 0.05 and P < 0.01, respectively), suggesting stimulation of early follicular recruitment (Fig. 3C).
Multilaminar-primary follicle counts were significantly elevated in PNX 5 (16.8 ± 1.9%) and PNX 30 (14.7 ± 2.2%) groups compared to both PCOS (9.4 ± 1.4%) and control groups (8.6 ± 1.1%) (P < 0.05 and P < 0.01, respectively), suggesting stimulation of early follicular recruitment (Fig. 3C).
Treatment with PNX-14 at 2.5 nmol significantly reduced atresia (7.0 ± 1.1; P < 0.01), with similar improvements at 5 and 30 nmol (Fig. 3H).
While the PNX-14 (2.5 nmol) group showed a mild increase (0.73 ± 0.05-fold), the PNX-14 (5 nmol) group demonstrated a moderate restoration of PCNA levels (0.91 ± 0.07-fold). In contrast, the PNX-14 (30 nmol) group displayed lower PCNA expression (0.65 ± 0.08-fold).
While the PNX-14 (2.5 nmol) group showed a mild increase (0.73 ± 0.05-fold), the PNX-14 (5 nmol) group demonstrated a moderate restoration of PCNA levels (0.91 ± 0.07-fold). In contrast, the PNX-14 (30 nmol) group displayed lower PCNA expression (0.65 ± 0.08-fold).
While the PNX-14 (2.5 nmol) group showed a mild increase (0.73 ± 0.05-fold), the PNX-14 (5 nmol) group demonstrated a moderate restoration of PCNA levels (0.91 ± 0.07-fold). In contrast, the PNX-14 (30 nmol) group displayed lower PCNA expression (0.65 ± 0.08-fold).
Citation and release provenance
Cite this identity as PepDiana record PEPDIA-PLP-000501, release PepDiana-V1-20260620. Experimental observations retain their paper, mention, and activity-record identifiers.
Record updated: 2026-06-22T07:14:26.229247+00:00