History of Andrographis
Andrographis Paniculata is an
annual herbaceous plant in the family Acanthaceae, and is one of the
most commonly used medicinal plants in the traditional systems of
Traditional Chinese and Ayurvedic medicines. It is widely cultivated in
India, China, and Southeastern Asia.
A. paniculata have shown a broad
range of pharmacological effects such as anti-viral, antibacterial,
prevention of common cold, anti-diarrheal, support healthy blood
glucose, and support healthy inflammatory response.
It is know as the “king of bitters”
due to its bitter flavor profile. Andrographolide, an active ingredient
in Andrographis, has
been shown to be responsible for the herb's inflammatory modulating
ParActin® is a patented
extract of Andrographis Paniculata, standardized to Andrographolide,
and Neoandrographolide. (US Patent No: 8,084,495 B2) Preliminary
research has shown ParActin® to promote healthy
inflammatory response by naturally invigorating the PPAR gamma response,
inhibiting NF-kappaB, the key regulator of our
inflammatory response system, thereby naturally reducing
pro-inflammatory cytokines and proteins associated with pain
and redness from everyday activities.
Benefits of ParActin®
- Supports Healthy
- Supports Healthy Joint
- Supports Healthy Immune
- Supports Healthy Brain
ParActin® Mode of Action
For Joint Health
ParActin® Works By:
- Inhibits NF-κB binding to DNA
- Inhibits IKKβ
- Inhibits COX-2 and reduce
- Inhibits NFAT – bone erosion
- Stimulates osteoblasts &
- Decreases Rheumatoid Factor -
- Reduces IgA & IgM: cartilage
- Reduces C-Reactive Protein
- Promote regulatory T cell (Treg),
- Reduces AP-1 & STAT3 in
NF-kB and NFAT are key regulator
of our immune and inflammatory response system. Research has shown NF-kB
to be activated in rheumatoid synovium cells. Both in vitro and in vivo
research showed ParActin® to inhibit NF-kB activity and
reduced the DNA binding of NF-kB, thereby reducing IL-2, COX-2, and
PGE2. In vitro study also showed ParActin® to inhibit NFAT
activity, a transcription factor linked with bone erosion. ParActin®
also induces osteoblast mineralization on the bones via COX-2
expression, which could be of useful in preventing osteoporosis.
Efficacy Findings from
ParActin® Joint Health Clinical Trials
In a randomized, double blind, and
placebo-controlled study published on Clinical Rheumatology 2009, 60
patients with rheumatoid arthritis were given 100mg of ParActin®
or placebo three times a day for 14 weeks in conjunction with MTX.
Showed Significant Diminishing In:
- number of swollen joints (Paractin
9 vs Placebo 13)
- total grade of swollen
joint (Paractin 11 vs Placebo 16)
- total grade of tender
joints (Paractin 14 vs Placebo 17)
- HAQ (Paractin 19 vs
- reduction of rheumatoid
factor (Paractin 119 vs Placebo 130)
- reduction in IgA (Paractin
293.7 vs placebo 335)
ParActin® was effective
in reducing number of swollen joints, total grade of swollen joint and
tender joints. ParActin® help normalize Rheumatoid Factor,
creatinkinase, hemoglobin, immunoglobin IgA and IgM. The reduction in
IgA and IgM is beneficial as there is positive correlation between the
grade of cartilage damage.
In another clinical published on
Innovative Rheumatology Jan 2013, 8 patients with various rheumatoid
conditions were given 300mg of ParActin® daily for 3 ½ years.
Treatment with ParActin® showed significant improvement in
number of swollen joints, total grade of swollen joint, total grade of
tender joints, and improvement in Quality of Life. In addition, we are
seeing significant reduction in Rheumatoid Factor, Eryhrocytes
Sedimentation Rate, Pain, and C-Reactive Protein.
ParActin® Reduces Rheumatoid
ParActin® significantly reduced the RF value from 110 to 70
The placebo group, did not experience any significant change in RF
Innovative Rheumatology Jan
In another clinical published on Innovative Rheumatology Jan 2013, 8
patients with various rheumatoid conditions were given 300mg of ParActin®
daily for 4 years.
Treatment with ParActin® showed significant improvement
in number of swollen joints, total grade of swollen joint, total grade
of tender joints, and improvement in Quality of Life. In addition, we
are seeing significant reduction in Rheumatoid Factor, Erythrocytes
Sedimentation Rate, and C-Reactive Protein.
Serum immunological parameters of inflammation were
reduced progressively during 48 month of ParActin® treatment. After 24
months the treatment with Paractin®, 6 patients were administered only
with ParActin® as monotherapy. All patients are showing full
tolerability, no remission of clinical and serological inflammatory
Significant Reduction in
Rheumatoid Factors and C-Reactive Protein
Reduction in Fatigue & Pain
ParActin® Beneficial for Bone Health
In the process of bone formation, osteoblasts produce a calcium and
phosphate-based mineral that is deposited. Almost the entire bone matrix
is mineralized by the osteoblasts. An osteoclast is a type of bone cell
that resorbs and break down bone tissue. Balance of bone formation and
bone resorption tends to be negative with age, particularly in
post-menopausal women, often leading to a loss of bone serious enough to
cause fractures, which is called osteoporosis. ParActin® increase
osteoblast and has a mineralizing effect on the bones with the increase
of calcium ddeposits. Therefore, it could be
beneficial in osteoporosis.
ParActin® Increase Osteoblast
Via COX-2 mRNA Expression
ParActin® Has Mineralizing
Increasing Calcium Deposits In TheBones
ParActin® For Muscle Health
In a research published on Skeletal Muscle 2014, we investigated the
effects of ParActin® on the onset of dystrophy in mdx mice, an animal
model used to study MD.
ParActin® Reduces Muscle Damage and Lowered
Serum Creatine Kinase
Administration of ParActin® reduced necrosis, and cumulative muscle
damage compared with vehicle-treated mdx mice. Concordantly, serum CK
levels were decreased in ParActin® treated mdx mice compared with
control mdx mice, with an approximately 50% recovery score.
ParActin® Reduces Fibrosis: Fibronectin and
Development of fibrosis in is characterized by an increase in
extracellular matrix compounds such as fibronectin and several types of
collagen. ParActin® treatment decreased fibronectin and collagen III
protein levels. ParActin® treated mice exhibited less severe muscular
dystrophy, performed better in an exercise endurance test, and had
improved muscle strength compared to untreated mdx mice.
ParActin® Reduces Pro-Fibrotic Factor: TGF-b,
b, b, b, CTGF, and Collagen Type I
ParActin® treatment reduced TGF-β, an important pro-fibrotic
factor in mdx skeletal muscle. In addition, Connective tissue growth
factor (CTGF) and collagen type I, two downstream pro-fibrotic factors
in dystrophic skeletal muscle were also reduced by ParActin® treatment.
ParActin® Improves Skeletal Muscle Strength
and Exercise Performance
ParActin®-treated mdx mice showed an enhanced exercise
performance, significant increase in the generation of isometric force,
and higher strength in the TA muscle. This is evidenced by a significant
decrease in the number of detentions in the treadmill running protocol,
with recovery score of 45.5%.
Mode of Action for Brain Health
ParActin® Works By:
- Activates both canonical and
non-canonical Wnt signaling
- Inhibits GSK-3β
- Reduces tau
- Activates Peroxisome
- Induces postsynaptic proteins
and synaptic function (LTP)
- Stimulates Neurogenesis
Learning and Memory
In the Morris Mice Water Maze Experiment, the mice were trained in a
circular pool to locate the escape platform. Transgenic mice treated
with ParActin® showed improve learning and memory. The lower
escape latency values indicate that ParActin® was able to
reduce the cognitive impairment in the spatial memory performance.
ParActin® alleviates memory decline by inducing postsynaptic
proteins and synaptic function in the transgenic mice. In addition,
ParActin® prevents the inflammatory oxidative stress and tau
phosphorylation in the hipocamppus.
Tau protein stabilizes
microtubules and is abundantly present in brain. Beta amyloid induces
the occurrence of phospho-epitopes in tau protein associated with
neuronal damage. When Tau protein is defective, they no longer
stabilizes microtubules properly and can result in dementia such as
Alzheimer. ParActin® prevents tau hyperphosphorylation,
increases field excitatory postsynaptic potentials, and inhibits
long-term depression (LTD) via the inhibition of the glycogen synthase
Wnt Signaling By Inhibition of GSK-3β & Stimulates Neurogenesis
kinase-3β is an enzyme that regulates Wnt signaling pathway, gene
transcription, and neuronal cell function. The Wnt/β-catenin signaling
pathway is essential in the nervous system and participates in the
neural tube formation and midbrain development. Blocked Wnt pathway
caused reduced neurogenesis and impaired learning and memory function.
ParActin® activates Wnt signaling pathway by a mechanism that
bypasses the Wnt receptor and involves inhibition of GSK-3β. In silico
analyses ParActin® directly inhibits GSK-3β by competing at the
substrate binding site.
In vivo research showed that
treatment of 2 month-old wild-type mice treated with ParActin®
for 4 weeks strongly induces cell proliferation and the generation of
newborn neurons in the dentate gyrus, increases density of immature
neurons, increases percentage of the granular cell layer, more complex
morphology, and induces development of newborn neurons.
- María A. Hidalgo,
Juan L. Hancke, Juan C. Bertoglio, and Rafael A. Burgos.
Andrographolide a New Potential Drug for the Long Term Treatment of
Rheumatoid Arthritis Disease. Innovative Rheumatology, January 2013
- Burgos, R. A, Hancke,
J. L, Bertoglio, J. C, Aguirre, V, Arriagada, S, Calvo, M, et al.
Efficacy of an Andrographis paniculata composition for the relief of
rheumatoid arthritis symptoms: a prospective randomized
placebo-controlled trial. Clin Rheumatol. (2009), 28(8), 931-46.
- Burgos, R. A,
Hidalgo, M. A, Carretta, M. D, Bertoglio, J. C, Folch, H, & Hancke,
J. L. Immunomodulatory activities induced by Andrographis paniculata.
Studium Press LLC; (2009).
- Mirentxu I.
Iruretagoyena, Claudio A. Figueroa, Rafael A. Burgos, Juan L. Hancke.
Andrographolide interferes with T cell activation and reduces
experimental autoimmune encephalomyelitis in the mouse. J Pharmacol
Exp Ther. (2005). , 312(1), 366-72.
- Burgos, R. A, Seguel,
K, Perez, M, Meneses, A, Ortega, M, Guarda, M. I, et al.
Andrographolide inhibits IFN-gamma and IL-2 cytokine production and
protects against cell apoptosis. Planta Med. (2005). , 71(5),
- Hidalgo, M. A,
Romero, A, Figueroa, J, Cortes, P, Concha, I. I, Hancke, J. L, et
al. Andrographolide interferes with binding of nuclear factor-kappaB
to DNA in HL-60-derived neutrophilic cells. Br J Pharmacol. (2005).
, 144(5), 680-6.
For more information on PARACTIN®
* The products and the
information provided have not been evaluated by the Food and Drug
administration. The product is not intended to diagnose, treat, cure, or
prevent any disease.