Cartalax 20mg

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Size Options: 20mg Composition: Fragment 176-191 Form: Lyophilized Powder Purity: >99% Product Code: P-FRAG176-191

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Description

Cartalax 20mg

Cartalax, also known as AED or T-31 peptide, is a synthetic peptide crafted to target specific biological pathways associated with cellular aging. This peptide is derived from the amino acid sequence found in the alpha-1 chain of type XI collagen, represented by the acronym AED (Alanine-Glutamate-Aspartate), and has been isolated from kidney extracts containing polypeptides. Peptides like Cartalax are the subject of extensive research due to their potential to influence biological processes, including inflammation and cartilage repair, which are crucial in conditions like osteoarthritis. Cartalax falls under the category of Khavinson peptides and is being explored for its bioregulatory properties.

Research and Clinical Studies

The following sections summarize recent findings from studies investigating Cartalax’s potential effects on various aspects of cellular aging.

Cartalax and Fibroblasts

In the realm of cellular biology, the Cartalax peptide has emerged as a potential game-changer, particularly in its interactions with skin fibroblasts. These interactions hint at Cartalax’s capacity to wield a profound influence on the aging process of these cells when cultivated in a laboratory setting.

One of the standout properties of Cartalax lies in its potential to stimulate the proliferation of fibroblasts. This assertion is rooted in its observed ability to enhance the expression of Ki-67, a renowned marker closely associated with cell proliferation. In aging fibroblast cultures, it’s a common phenomenon for Ki-67 expression to decline. However, Cartalax appears to counter this trend, suggesting that it might stimulate fibroblast growth or extend their replicative lifespan. In essence, Cartalax seems poised to combat the natural decline in cell division that typically accompanies the aging process.

Beyond its impact on proliferation, Cartalax’s influence on the expression of CD98hc (a glycoprotein) is of paramount significance. CD98hc plays a pivotal role in cellular regeneration and aging processes. The heightened expression of CD98hc in the presence of Cartalax hints at its potential to augment the regenerative capacity of aging fibroblasts. This could translate to sustained vitality among aging cells, preserving cellular functions that often diminish with age.

Apoptosis, or programmed cell death, is a fundamental aspect of tissue renewal and homeostasis. However, an excessive or dysregulated increase in apoptosis can be detrimental, particularly during the aging of cell cultures. Cartalax emerges as a potential guardian against this dilemma. It appears to suppress caspase-3 activity, a marker associated with apoptosis. By doing so, Cartalax might enable fibroblasts to evade the heightened risk of cell death associated with aging, potentially extending their cellular lifespan. Notably, researchers have noted that Cartalax effectively reduced apoptosis levels in both young and aged cell cultures.

Cartalax doesn’t stop at influencing cellular processes; it also demonstrates the ability to inhibit the synthesis of MMP-9, an enzyme intricately involved in extracellular matrix remodeling. Elevated MMP-9 activity is a common hallmark of aging in fibroblasts. By curtailing MMP-9 synthesis, Cartalax holds the potential to safeguard the integrity of the extracellular matrix, potentially averting or mitigating the degenerative changes typically associated with aging.

In essence, Cartalax emerges as a multifaceted regulator, impacting various markers in a replicative aging model of skin fibroblasts, including Ki-67 (associated with proliferation), CD98hc (a glycoprotein), Caspase-3 (a marker of apoptosis), and MMP9 (involved in extracellular matrix degradation). These findings offer intriguing insights, suggesting that Cartalax’s reparative potential may extend beyond fibroblasts, potentially benefiting cartilage tissues as well. As chondrocytes (cartilage cells) share structural and functional similarities with fibroblasts, Cartalax’s promise in influencing cellular aging could hold significant implications for tissue repair and rejuvenation.

In conclusion, the interaction between Cartalax and fibroblasts presents a compelling avenue for further research into the intricate mechanisms governing cellular aging and the potential for therapeutic interventions to enhance cell health and longevity.

Cartalax and Kidney Cells

Cartalax, a peptide, holds promise in positively influencing the regeneration of kidney cells based on compelling research findings. In studies conducted on organotypic kidney tissue cultures obtained from both young and older murine models, the presence of Cartalax has been associated with a notable increase in cellular proliferation. This heightened proliferation is evident through the upregulation of Ki-67, a widely recognized marker used to assess cell proliferation levels.

Furthermore, Cartalax demonstrates the potential to reduce apoptotic processes within kidney cells. It achieves this by down-regulating the expression of p53, a proapoptotic protein known to facilitate cell death when expressed at elevated levels. The modulation of p53 by Cartalax suggests that this peptide may contribute to maintaining cellular integrity and extending cell survival, offering a promising avenue for addressing the aging process of kidney cells.

Additional studies, including investigations involving aging renal cell cultures, provide further support for Cartalax’s potential impact. These studies propose that Cartalax may exert its influence by promoting cell proliferation and potentially modifying the expression of crucial markers associated with aging. Specifically, Cartalax is believed to have the capacity to decrease the expression of aging-related markers such as p16, p21, and p53, proteins frequently implicated in cellular senescence—the state in which cells cease their division and growth.

Moreover, Cartalax is suggested to enhance the expression of SIRT-6, a protein renowned for its role in DNA repair and the maintenance of genomic stability, processes known to decline with age. The promotion of SIRT-6 expression by Cartalax may play a vital role in slowing down the aging process within renal cells, as diminished SIRT-6 levels are associated with accelerated cellular aging.

Notably, the protective effects of Cartalax on kidney cells may stem from its interactions with DNA. Research indicates that Cartalax can form energetically favorable complexes with specific DNA sequences, particularly d(ATATATATAT)2 within the minor groove. This interaction is hypothesized to serve as a catalyst for changes in gene expression, including genes responsible for aging markers in renal cells. By potentially modulating gene expression, Cartalax may contribute to preserving the health and function of kidney cells, potentially delaying the aging process.

The intricate interplay between Cartalax and kidney cells revealed through experimental data models sheds light on the complexities of these mechanisms. The proposition that Cartalax’s interaction with DNA may lead to alterations in gene expression offers a novel perspective on how specific peptides can influence the molecular aspects of the aging process. These findings pave the way for further exploration and potential interventions aimed at enhancing the longevity and vitality of kidney cells.

Cartalax and Cellular Aging

Aside from its potential effects on fibroblasts and kidney cell cultures, Cartalax has also undergone scrutiny for its potential impact on bone marrow mesenchymal stem cells and their connection to the aging process. This investigation is grounded in an examination of gene expression levels in cells experiencing aging under two distinct conditions: “passages,” during their proliferation phase, and “stationary” conditions, representing non-proliferating states. In the context of cell culture, the term “passages” is used to denote the number of times cells have been divided and subcultured. Eventually, cells enter a “stationary” growth phase, often associated with cellular senescence, wherein they no longer divide but remain metabolically active, mirroring the cellular aging process.

Cartalax is suggested to play a role in upregulating the insulin-like growth factor 1 (IGF1) gene in both aging models, potentially amplifying its expression by approximately 3.5 to 5.6 times. IGF1 is a well-known protein involved in cellular growth and development. The heightened expression of IGF1, driven by Cartalax, implies a potential role for the peptide in enhancing growth-related cellular functions, which could counteract specific aspects of cellular aging. Additionally, the study highlights an eightfold increase in the expression of the TERT gene in “stationary” aging conditions. Although the provided text does not specify Cartalax’s direct influence on TERT expression, it is noteworthy as TERT encodes the catalytic subunit of telomerase—an enzyme critical for maintaining telomere length and, consequently, cellular longevity. Any potential modulation of TERT by Cartalax could carry significant implications for cellular aging.

Furthermore, Cartalax appears to stimulate the expression of the NFκB gene in both aging models. NFκB is a protein complex involved in various cellular processes, including inflammation, immunity, and cellular survival. The activation of NFκB by Cartalax suggests its potential impact on cellular stress response pathways closely tied to the aging process. Additionally, the study highlights that Cartalax does not influence TNKS2 in “passages” but inhibits it in “stationary” aging cultures. TNKS2, or Tankyrase 2, is a member of the poly(ADP-ribose) polymerase (PARP) enzyme family, known to regulate various cellular processes, including Wnt signaling, telomere maintenance, and vesicle trafficking. Notably, telomere maintenance is considered instrumental in the potential anti-aging effects of Cartalax’s interaction with TNKS2.

In summary, Cartalax’s exploration in the realm of cellular aging extends to bone marrow mesenchymal stem cells. Its observed effects on gene expression, especially in “stationary” conditions, suggest the peptide’s potential to modulate crucial factors associated with cellular aging, such as IGF1, TERT, and NFκB. Additionally, Cartalax’s interaction with TNKS2 holds promise for influencing telomere maintenance and mitigating the aging process at a molecular level. These findings offer intriguing avenues for further research into interventions aimed at promoting cellular longevity and addressing age-related cellular changes.

 

CAS Number 
SequenceAla-Glu-Asp
Molecular Weight333.3 g/mol
Molecular FormulaC12H19N3O8
SynonymsAED, T-31, SCHEMBL5324601
Storage (Lyophilized)

At 39 Fahrenheit: 2 years

At -4 Fahrenheit: 3 years

 

Cartalax 20mg

Cartalax, also known as AED or T-31 peptide, is a synthetic peptide crafted to target specific biological pathways associated with cellular aging. This peptide is derived from the amino acid sequence found in the alpha-1 chain of type XI collagen, represented by the acronym AED (Alanine-Glutamate-Aspartate), and has been isolated from kidney extracts containing polypeptides. Peptides like Cartalax are the subject of extensive research due to their potential to influence biological processes, including inflammation and cartilage repair, which are crucial in conditions like osteoarthritis. Cartalax falls under the category of Khavinson peptides and is being explored for its bioregulatory properties.

Research and Clinical Studies

The following sections summarize recent findings from studies investigating Cartalax’s potential effects on various aspects of cellular aging.

Cartalax and Fibroblasts

In the realm of cellular biology, the Cartalax peptide has emerged as a potential game-changer, particularly in its interactions with skin fibroblasts. These interactions hint at Cartalax’s capacity to wield a profound influence on the aging process of these cells when cultivated in a laboratory setting.

One of the standout properties of Cartalax lies in its potential to stimulate the proliferation of fibroblasts. This assertion is rooted in its observed ability to enhance the expression of Ki-67, a renowned marker closely associated with cell proliferation. In aging fibroblast cultures, it’s a common phenomenon for Ki-67 expression to decline. However, Cartalax appears to counter this trend, suggesting that it might stimulate fibroblast growth or extend their replicative lifespan. In essence, Cartalax seems poised to combat the natural decline in cell division that typically accompanies the aging process.

Beyond its impact on proliferation, Cartalax’s influence on the expression of CD98hc (a glycoprotein) is of paramount significance. CD98hc plays a pivotal role in cellular regeneration and aging processes. The heightened expression of CD98hc in the presence of Cartalax hints at its potential to augment the regenerative capacity of aging fibroblasts. This could translate to sustained vitality among aging cells, preserving cellular functions that often diminish with age.

Apoptosis, or programmed cell death, is a fundamental aspect of tissue renewal and homeostasis. However, an excessive or dysregulated increase in apoptosis can be detrimental, particularly during the aging of cell cultures. Cartalax emerges as a potential guardian against this dilemma. It appears to suppress caspase-3 activity, a marker associated with apoptosis. By doing so, Cartalax might enable fibroblasts to evade the heightened risk of cell death associated with aging, potentially extending their cellular lifespan. Notably, researchers have noted that Cartalax effectively reduced apoptosis levels in both young and aged cell cultures.

Cartalax doesn’t stop at influencing cellular processes; it also demonstrates the ability to inhibit the synthesis of MMP-9, an enzyme intricately involved in extracellular matrix remodeling. Elevated MMP-9 activity is a common hallmark of aging in fibroblasts. By curtailing MMP-9 synthesis, Cartalax holds the potential to safeguard the integrity of the extracellular matrix, potentially averting or mitigating the degenerative changes typically associated with aging.

In essence, Cartalax emerges as a multifaceted regulator, impacting various markers in a replicative aging model of skin fibroblasts, including Ki-67 (associated with proliferation), CD98hc (a glycoprotein), Caspase-3 (a marker of apoptosis), and MMP9 (involved in extracellular matrix degradation). These findings offer intriguing insights, suggesting that Cartalax’s reparative potential may extend beyond fibroblasts, potentially benefiting cartilage tissues as well. As chondrocytes (cartilage cells) share structural and functional similarities with fibroblasts, Cartalax’s promise in influencing cellular aging could hold significant implications for tissue repair and rejuvenation.

In conclusion, the interaction between Cartalax and fibroblasts presents a compelling avenue for further research into the intricate mechanisms governing cellular aging and the potential for therapeutic interventions to enhance cell health and longevity.

Cartalax and Kidney Cells

Cartalax, a peptide, holds promise in positively influencing the regeneration of kidney cells based on compelling research findings. In studies conducted on organotypic kidney tissue cultures obtained from both young and older murine models, the presence of Cartalax has been associated with a notable increase in cellular proliferation. This heightened proliferation is evident through the upregulation of Ki-67, a widely recognized marker used to assess cell proliferation levels.

Furthermore, Cartalax demonstrates the potential to reduce apoptotic processes within kidney cells. It achieves this by down-regulating the expression of p53, a proapoptotic protein known to facilitate cell death when expressed at elevated levels. The modulation of p53 by Cartalax suggests that this peptide may contribute to maintaining cellular integrity and extending cell survival, offering a promising avenue for addressing the aging process of kidney cells.

Additional studies, including investigations involving aging renal cell cultures, provide further support for Cartalax’s potential impact. These studies propose that Cartalax may exert its influence by promoting cell proliferation and potentially modifying the expression of crucial markers associated with aging. Specifically, Cartalax is believed to have the capacity to decrease the expression of aging-related markers such as p16, p21, and p53, proteins frequently implicated in cellular senescence—the state in which cells cease their division and growth.

Moreover, Cartalax is suggested to enhance the expression of SIRT-6, a protein renowned for its role in DNA repair and the maintenance of genomic stability, processes known to decline with age. The promotion of SIRT-6 expression by Cartalax may play a vital role in slowing down the aging process within renal cells, as diminished SIRT-6 levels are associated with accelerated cellular aging.

Notably, the protective effects of Cartalax on kidney cells may stem from its interactions with DNA. Research indicates that Cartalax can form energetically favorable complexes with specific DNA sequences, particularly d(ATATATATAT)2 within the minor groove. This interaction is hypothesized to serve as a catalyst for changes in gene expression, including genes responsible for aging markers in renal cells. By potentially modulating gene expression, Cartalax may contribute to preserving the health and function of kidney cells, potentially delaying the aging process.

The intricate interplay between Cartalax and kidney cells revealed through experimental data models sheds light on the complexities of these mechanisms. The proposition that Cartalax’s interaction with DNA may lead to alterations in gene expression offers a novel perspective on how specific peptides can influence the molecular aspects of the aging process. These findings pave the way for further exploration and potential interventions aimed at enhancing the longevity and vitality of kidney cells.

Cartalax and Cellular Aging

Aside from its potential effects on fibroblasts and kidney cell cultures, Cartalax has also undergone scrutiny for its potential impact on bone marrow mesenchymal stem cells and their connection to the aging process. This investigation is grounded in an examination of gene expression levels in cells experiencing aging under two distinct conditions: “passages,” during their proliferation phase, and “stationary” conditions, representing non-proliferating states. In the context of cell culture, the term “passages” is used to denote the number of times cells have been divided and subcultured. Eventually, cells enter a “stationary” growth phase, often associated with cellular senescence, wherein they no longer divide but remain metabolically active, mirroring the cellular aging process.

Cartalax is suggested to play a role in upregulating the insulin-like growth factor 1 (IGF1) gene in both aging models, potentially amplifying its expression by approximately 3.5 to 5.6 times. IGF1 is a well-known protein involved in cellular growth and development. The heightened expression of IGF1, driven by Cartalax, implies a potential role for the peptide in enhancing growth-related cellular functions, which could counteract specific aspects of cellular aging. Additionally, the study highlights an eightfold increase in the expression of the TERT gene in “stationary” aging conditions. Although the provided text does not specify Cartalax’s direct influence on TERT expression, it is noteworthy as TERT encodes the catalytic subunit of telomerase—an enzyme critical for maintaining telomere length and, consequently, cellular longevity. Any potential modulation of TERT by Cartalax could carry significant implications for cellular aging.

Furthermore, Cartalax appears to stimulate the expression of the NFκB gene in both aging models. NFκB is a protein complex involved in various cellular processes, including inflammation, immunity, and cellular survival. The activation of NFκB by Cartalax suggests its potential impact on cellular stress response pathways closely tied to the aging process. Additionally, the study highlights that Cartalax does not influence TNKS2 in “passages” but inhibits it in “stationary” aging cultures. TNKS2, or Tankyrase 2, is a member of the poly(ADP-ribose) polymerase (PARP) enzyme family, known to regulate various cellular processes, including Wnt signaling, telomere maintenance, and vesicle trafficking. Notably, telomere maintenance is considered instrumental in the potential anti-aging effects of Cartalax’s interaction with TNKS2.

In summary, Cartalax’s exploration in the realm of cellular aging extends to bone marrow mesenchymal stem cells. Its observed effects on gene expression, especially in “stationary” conditions, suggest the peptide’s potential to modulate crucial factors associated with cellular aging, such as IGF1, TERT, and NFκB. Additionally, Cartalax’s interaction with TNKS2 holds promise for influencing telomere maintenance and mitigating the aging process at a molecular level. These findings offer intriguing avenues for further research into interventions aimed at promoting cellular longevity and addressing age-related cellular changes.

 

CAS Number 
SequenceAla-Glu-Asp
Molecular Weight333.3 g/mol
Molecular FormulaC12H19N3O8
SynonymsAED, T-31, SCHEMBL5324601
Storage (Lyophilized)

At 39 Fahrenheit: 2 years

At -4 Fahrenheit: 3 years

 

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