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P021

Peptide 021, GLXC-21260

A tetrapeptide derived from CNTF, designed to promote neurogenesis, enhance cognition, and mitigate Alzheimer's pathologies by modulating neurotrophic signaling.

Quick Stats
Studies 37
Trials 57
Formula C27H42N6O8
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Utility 3
pubmed Jul 15, 2014

Disease modifying effect of chronic oral treatment with a neurotrophic peptidergic compound in a triple transgenic mouse model of Alzheimer's disease.

Kazim. Syed Faraz SF; Blanchard. Julie J; Dai. Chun-Ling CL; Tung. Yunn-Chyn YC; LaFerla. Frank M FM...

In a mouse model of Alzheimer’s, giving the oral peptide P021 for a year lowered harmful tau protein changes, slightly reduced soluble amyloid‑beta, boosted brain‑derived neurotrophic factor, and improved memory and brain cell growth, suggesting the peptide might help slow disease progression.

Utility 3
pubmed Jul 11, 2016

Neurotrophic factor small-molecule mimetics mediated neuroregeneration and synaptic repair: emerging therapeutic modality for Alzheimer's disease.

Kazim. Syed Faraz SF; Iqbal. Khalid K

Peptide P021 is a tiny, brain‑penetrating compound that mimics natural growth factors and, in animal studies, boosts new brain cell growth, improves memory, and cuts down harmful tau protein changes linked to Alzheimer’s. It works by raising BDNF levels and calming a pathway that normally adds bad phosphate tags to tau. So far it’s only been tested in mice, but it looks safe and can be taken by mouth.

Utility 3
pubmed Mar 2, 2014

Rescue of cognitive-aging by administration of a neurogenic and/or neurotrophic compound.

Bolognin. Silvia S; Buffelli. Mario M; Puoliväli. Jukka J; Iqbal. Khalid K

Giving rats a small peptide called P021 by mouth for a long time helped older rats keep their memory and learning abilities. The peptide boosted brain growth factors, improved the creation of new brain cells, fixed synapse problems, and lowered a brain chemical (myoinositol) that usually goes up with age.

Utility 3
pubmed Apr 20, 2016

36th International Symposium on Intensive Care and Emergency Medicine : Brussels, Belgium. 15-18 March 2016.

Bateman. R. M. RM; Sharpe. M. D. MD; Jagger. J. E. JE; Ellis. C. G. CG; Solé-Violán. J. J;...

This pilot study looked at presepsin, a blood protein that rises when you have sepsis. The researchers measured how quickly presepsin levels go up and down in patients with severe infections and checked if those numbers could predict who would get better or worse.

Utility 3
pubmed Nov 19, 2019

Inhibition of AMD-Like Pathology With a Neurotrophic Compound in Aged Rats and 3xTg-AD Mice.

Liu. Yinghua Y; Wei. Wei W; Baazaoui. Narjes N; Liu. Fei F; Iqbal. Khalid K

A study in old rats and Alzheimer-model mice showed that a brain‑supporting peptide called P021, taken regularly for several months, reduced eye damage that looks like age‑related macular degeneration (AMD). The peptide lowered signs of cell loss, inflammation, and protein buildup in the retina, suggesting it might help keep vision healthier as we age.

Utility 2
pubmed Oct 2, 2022

Alzheimer's Disease: Challenges and a Therapeutic Opportunity to Treat It with a Neurotrophic Compound.

Baazaoui. Narjes N; Iqbal. Khalid K

The abstract talks about a tiny protein fragment called P021 that mimics brain‑helping factors and can get into the brain more easily than whole proteins. In animal studies it boosted brain cell growth, improved memory‑related pathways, and reduced Alzheimer‑type damage, suggesting it could become a future drug for dementia. However, it’s still only tested in labs, not in people, so there’s no dosage or safety guide for everyday use yet.

Utility 2
pubmed 2017

Prevention of Amyloid-β and Tau Pathologies, Associated Neurodegeneration, and Cognitive Deficit by Early Treatment with a Neurotrophic Compound.

Baazaoui. Narjes N; Iqbal. Khalid K

In a mouse model of Alzheimer’s, giving the neurotrophic peptide P021 early (before any brain damage shows up) stopped the buildup of harmful amyloid‑beta and tau proteins, protected brain cells, kept memory performance normal, and lowered death rates. The study shows that boosting brain‑cell health early can prevent Alzheimer‑type changes in mice, but it’s still far from proven in people.

Utility 2
pubmed 2021

Neurotrophic Treatment Initiated During Early Postnatal Development Prevents the Alzheimer-Like Behavior and Synaptic Dysfunction.

Wei. Wei W; Liu. Yinghua Y; Dai. Chun-Ling CL; Baazaoui. Narjes N; Tung. Yunn Chyn YC; Liu. Fei F; I...

In a mouse model of Alzheimer’s, giving the peptide P021 from birth until about four months old stopped memory problems and helped keep brain connections healthy. The peptide boosted brain chemicals that support learning and memory, like BDNF, and fixed deficits in proteins needed for synapses.

Utility 2
pubmed Aug 27, 2020

Prenatal to early postnatal neurotrophic treatment prevents Alzheimer-like behavior and pathology in mice.

Wei. Wei W; Wang. Yifan Y; Liu. Yinghua Y; Dai. Chun-Ling CL; Tung. Yunn-Chyn YC; Liu. Fei F; Iqbal....

Giving a brain‑supporting peptide (P021) to pregnant mice and their babies prevented memory problems and Alzheimer‑type brain changes when they grew up, showing that early neurotrophic help can influence later disease risk. However, this is an animal study and not ready for human use yet.

Utility 2
pubmed Jan 19, 2001

Reduction of [Ca(2+)](i) restores uncoupled beta-adrenergic signaling in isolated perfused transgenic mouse hearts.

Serikov. V B VB; Petrashevskaya. N N NN; Canning. A M AM; Schwartz. A A

The study found that when the calcium level in the fluid surrounding isolated mouse hearts was too high, the hearts didn’t respond well to beta‑adrenergic signals (the same signals that increase heart rate and strength). Dropping the calcium to a lower, more normal range restored the heart’s normal response. This was true in three different genetically altered mouse models.

Utility 2
pubmed May 10, 2019

Serotype and molecular diversity of nasopharyngeal Streptococcus pneumoniae isolates from children before and after vaccination with the ten-valent pneumococcal conjugate vaccine (PCV10) in Ethiopia.

Sime. Wondewosen Tsegaye WT; Aseffa. Abraham A; Woldeamanuel. Yimtubezenash Y; Brovall. Sarah S; Mor...

The study looked at the types of bacteria living in kids’ noses in Ethiopia before and after they got the PCV10 vaccine. It found that the vaccine cut the amount of vaccine‑targeted strains by about half, but many other strains that the vaccine doesn’t cover became more common.

Utility 2
pubmed May 15, 2019

Validation of a Fast, Robust, Inexpensive, Two-Tiered Neonatal Screening Test algorithm on Dried Blood Spots for Spinal Muscular Atrophy.

Strunk. Annuska A; Abbes. Andre A; Stuitje. Antoine R AR; Hettinga. Chris C; Sepers. Eline M EM; Sne...

Scientists created a cheap, fast test that can spot babies who lack the SMN1 gene, which causes spinal muscular atrophy (SMA). The test works on dried blood spots, is 100% accurate in the study, and can also tell how many copies of the related SMN2 gene a patient has. While this is great for newborn screening programs, it doesn't directly change how most biohackers or self‑experimenters manage their own health.

Utility 2
pubmed Jul 14, 2022

Nitrobenzoate-Derived Compound X8 Impairs Vascular Development in Zebrafish.

Chiu. Chien-Chih CC; Chin. Hsieng-Kuo HK; Chung. Sen-Yuan SY; Hsieh. Kuan-Hsuan KH; Huang. Yi-Shan Y...

A new nitrobenzoate compound called X8 blocks blood vessel growth in zebrafish embryos. At a dose of 3 µM it causes malformed vessels, heart swelling, and circulation problems, likely by stopping cells from multiplying and moving and by lowering key vascular genes. The effect seems tied to interference with the VEGF/VEGFR2 pathway, which is a major driver of new blood vessel formation.

Utility 2
pubmed Dec 16, 2013

Comparison of salivary collection and processing methods for quantitative HHV-8 detection.

Speicher. D J DJ; Johnson. N W NW

The study shows that using the DNA Genotek P-021 saliva collection kit together with standard spin‑column DNA extraction lets you accurately measure virus levels in saliva, even after long‑term room‑temperature storage. This means you can reliably track viral DNA like HHV‑8 without needing a freezer, which is useful for low‑resource labs.

Utility 2
pubmed Sep 1, 2001

Stable therapeutic serum levels of human alpha-1 antitrypsin (AAT) after portal vein injection of recombinant adeno-associated virus (rAAV) vectors.

Song. S S; Embury. J J; Laipis. P J PJ; Berns. K I KI; Crawford. J M JM; Flotte. T R TR

Injecting a virus that carries the gene for human alpha‑1 antitrypsin (AAT) into the liver of mice can make the animals produce therapeutic levels of the protein in their blood, using far less virus than when the same gene is injected into muscle. The liver cells take up the gene, keep it as a circular DNA piece, and release the protein without harming the liver.

Utility 2
pubmed Nov 26, 2024

Effects of a ciliary neurotrophic factor (CNTF) small-molecule peptide mimetic in an in vitro and in vivo model of CDKL5 deficiency disorder.

Mottolese. Nicola N; Loi. Manuela M; Trazzi. Stefania S; Tassinari. Marianna M; Uguagliati. Beatrice...

The peptide P021 helped brain cells grow and survive in a dish made from CDKL5‑deficient cells, but when given to CDKL5‑deficient mice it did not raise BDNF levels, fix brain structure, or meaningfully improve behavior. More work is needed to see if starting treatment earlier or giving it longer could work.

Utility 2
pubmed May 25, 2020

DFIQ, a Novel Quinoline Derivative, Shows Anticancer Potential by Inducing Apoptosis and Autophagy in NSCLC Cell and In Vivo Zebrafish Xenograft Models.

Huang. Hurng-Wern HW; Bow. Yung-Ding YD; Wang. Chia-Yih CY; Chen. Yen-Chun YC; Fu. Pei-Rong PR; Chan...

DFIQ is a newly made quinoline chemical that kills lung cancer cells in lab dishes and in tiny fish that carry human tumors. It works by causing the cells to self‑destruct (apoptosis), damaging their DNA, and messing with their waste‑recycling system (autophagy) through a burst of harmful oxygen molecules. The study is still early‑stage and only in animals, so it isn’t ready for people to use yet.