FOR VETERINARY USE — Administer as directed by a licensed veterinarian. Shake well before use. Do not exceed recommended dose — calcium oversupplementation causes hypercalcaemia and can paradoxically impair bone mineralisation in growing puppies (particularly large and giant breeds where excess dietary calcium dysregulates the endochondral ossification process). Use under veterinary supervision in animals with renal impairment — reduced renal phosphorus excretion in chronic kidney disease (CKD) requires careful calcium-phosphorus balance management. Keep out of reach of children. Store in a cool, dry place away from direct sunlight.
Alembic Ascal Pet Calcium Tonic Syrup for Dogs & Cats | Calcium, Phosphorus & Vitamin D3 Supplement | Bone, Teeth, Growth & Lactation Support | 300ml
Alembic Ascal Pet is a veterinary calcium and mineral tonic syrup for dogs and cats, formulated to provide bioavailable calcium (as Calcium Gluconate and/or Calcium Lactate — confirm from product label), Phosphorus, and Vitamin D3 (Cholecalciferol) — the three essential nutrients that together regulate calcium homeostasis, support hydroxyapatite bone mineralisation, enable neuromuscular function, and maintain plasma calcium concentration within the narrow physiological range (2.2–2.9 mmol/L in dogs and cats). Ascal Pet is indicated for calcium deficiency states, growing puppies and kittens with high skeletal calcium demand, pregnant and lactating bitches at risk of eclampsia (puerperal hypocalcaemia), and senior pets with age-related bone density loss. Administer as directed by a licensed veterinarian.
Key Active Components & Mechanisms
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Calcium (as Calcium Gluconate and/or Calcium Lactate — confirm from Alembic Ascal Pet label) — the principal skeletal mineral and intracellular second messenger: Calcium is the most abundant mineral in the mammalian body (approximately 99% stored in the skeleton as hydroxyapatite — Ca10(PO4)6(OH)2 — the crystalline calcium phosphate mineral that provides the mechanical rigidity and compressive strength of cortical and trabecular bone); the remaining ~1% of total body calcium exists in the extracellular fluid (ionised Ca2+ at ~1.1–1.3 mmol/L free plasma concentration) and intracellular compartments where it functions as a critical second messenger in: (a) neuromuscular transmission — Ca2+ influx through voltage-gated Ca2+ channels (VGCC — specifically the L-type CaV1 channels at the presynaptic terminal) triggered by action potential depolarisation → Ca2+ binds synaptotagmin (the Ca2+ sensor on synaptic vesicles) → SNARE complex formation (syntaxin-1/SNAP-25/synaptobrevin) → synaptic vesicle fusion → acetylcholine release at the neuromuscular junction → muscle contraction; hypocalcaemia → reduced VGCC activation threshold → spontaneous action potentials → tetanic muscle contractions, tremors, and convulsions (classic signs of eclampsia/puerperal tetany in nursing bitches); (b) cardiac rhythm — Ca2+ via L-type channels is essential for the plateau phase (phase 2) of the cardiac ventricular action potential and for excitation-contraction coupling in cardiomyocytes (Ca2+-induced Ca2+ release from the SR via ryanodine receptors); (c) blood coagulation — Ca2+ (Factor IV) is required as a cofactor for multiple coagulation cascade serine proteases (Factors VII, IX, X, II prothrombin activation) that bind phosphatidylserine-exposing activated platelet membranes via γ-carboxyglutamate (Gla) domains in a Ca2+-bridged ternary complex; (d) bone mineralisation — osteoblast-secreted type I collagen osteoid matrix provides the template for hydroxyapatite crystal nucleation; Ca2+ and PO4 3− deposit into the osteoid matrix under the regulation of osteocalcin (a Gla-containing non-collagenous protein that binds Ca2+ in the mineralisation front, secreted by osteoblasts under Vitamin D3 and Vitamin K2 regulation) and osteopontin; the Ca:P ratio in the diet/supplement must approximate 1.2:1 to 1.4:1 for optimal bone mineralisation — excess phosphorus relative to calcium suppresses calcium absorption via intestinal precipitation and increases PTH-mediated bone resorption; dietary calcium is absorbed in the duodenum and proximal jejunum via two mechanisms: (i) transcellular active transport: Ca2+ enters enterocytes via the apical TRPV6 (transient receptor potential vanilloid 6 — the primary epithelial Ca2+ channel regulated by 1,25-dihydroxyvitamin D3/Calcitriol) → shuttled across the cytoplasm bound to Calbindin-D9k (an intracellular Ca2+ buffer that prevents toxic cytosolic Ca2+ elevation) → exported basolaterally by the plasma membrane Ca2+ ATPase (PMCA1b) and the Na+/Ca2+ exchanger (NCX1); this saturable, active transport pathway is the predominant calcium absorption route at low-to-normal dietary calcium intakes and is upregulated by Calcitriol (1,25-(OH)2D3 — the active form of Vitamin D3); (ii) paracellular passive diffusion: Ca2+ moves down its electrochemical gradient through the tight junction paracellular pathway — a non-saturable, non-regulated, low-efficiency pathway that becomes significant only at very high luminal calcium concentrations; Calcium Gluconate (Ca2+ salt of gluconic acid — readily soluble, good bioavailability, gentle on the GI mucosa — lower risk of GI irritation vs Calcium Chloride) and Calcium Lactate (Ca2+ salt of lactic acid — similar solubility and bioavailability to Gluconate) are organic calcium salts chosen for veterinary oral supplementation due to their superior GI tolerance and palatability vs inorganic salts
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Phosphorus — the skeletal co-mineral and energy metabolism central element: Phosphorus (as inorganic phosphate PO4 3−) comprises ~85% of body phosphorus in the skeleton as hydroxyapatite (co-deposited with calcium in the 1.67:1 Ca:P molar ratio of stoichiometric hydroxyapatite); the remaining ~15% is distributed as: (a) intracellular organic phosphate — ATP, ADP, AMP (adenosine phosphates — the universal cellular energy currency), NADH/NADPH, phospholipids (phosphatidylcholine, phosphatidylethanolamine, phosphatidylserine — membrane bilayer structural components), 2,3-bisphosphoglycerate (2,3-BPG — the allosteric haemoglobin oxygen affinity regulator in erythrocytes), and phosphorylated signalling intermediates (phosphotyrosine, phosphoserine, phosphothreonine on signal transduction proteins); (b) extracellular serum inorganic phosphate (Pi — normal range in dogs: 0.9–1.6 mmol/L; cats: 1.1–2.1 mmol/L) regulated by PTH (decreases renal Pi reabsorption → phosphaturia) and FGF-23 (fibroblast growth factor 23 — the osteocyte-secreted phosphaturic hormone that downregulates renal NaPi-IIa/NaPi-IIc sodium-phosphate cotransporters and also inhibits CYP27B1 → reduced 1,25-(OH)2D3 synthesis)
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Vitamin D3 (Cholecalciferol) — the endocrine regulator of calcium-phosphorus homeostasis (Ca2+/PO4 axis master hormone): Cholecalciferol (Vitamin D3) is a secosteroid prohormone synthesised in skin keratinocytes from 7-dehydrocholesterol via UV-B (290–315nm) photolysis → pre-Vitamin D3 → thermal isomerisation → Vitamin D3; absorbed dietary Vitamin D3 and skin-synthesised Vitamin D3 are transported in blood bound to Vitamin D-binding protein (DBP — Gc-globulin) → hepatic 25-hydroxylation by CYP2R1 (the primary hepatic Vitamin D 25-hydroxylase) → 25-hydroxyvitamin D3 (25-(OH)D3 — Calcidiol — the major circulating Vitamin D metabolite and the standard clinical measure of Vitamin D status) → renal 1α-hydroxylation by CYP27B1 (1α-hydroxylase — expressed in proximal tubular cells of the kidney, regulated by PTH, FGF-23, serum Ca2+, and 1,25-(OH)2D3 itself via negative feedback) → 1,25-dihydroxyvitamin D3 (1,25-(OH)2D3 — Calcitriol — the biologically active hormonal form); Calcitriol binds the nuclear Vitamin D receptor (VDR — a member of the nuclear receptor superfamily — NR1I1) → VDR-Calcitriol complex heterodimerises with the Retinoid X Receptor (RXRα — NR2B1) → VDR-RXR heterodimer binds Vitamin D Response Elements (VDREs — direct repeats of 5’-AGGTCA-3’ half-sites separated by 3bp spacers — DR3 motif) in the promoter regions of target genes → transcriptional regulation of: intestinal TRPV6 (apical Ca2+ entry channel upregulation → increased transcellular Ca2+ absorption), Calbindin-D9k (cytosolic Ca2+ buffer upregulation), PMCA1b (basolateral Ca2+ extrusion upregulation) → net increase in intestinal Ca2+ and PO4 3− absorption; renal Ca2+ reabsorption in distal convoluted tubule (TRPV5 channel upregulation); osteocalcin (bone Gla-protein — bone mineralisation regulator); and RANKL (receptor activator of NF-κB ligand — promotes osteoclast differentiation when needed for Ca2+ mobilisation from bone); net physiological outcome of Calcitriol: increased plasma Ca2+ and PO4 3− → provides substrate for hydroxyapatite bone mineralisation; Vitamin D3 (Cholecalciferol) is the preferred supplemental form vs Vitamin D2 (Ergocalciferol) in dogs and cats due to: higher potency and longer half-life of Cholecalciferol vs Ergocalciferol; cats in particular metabolise Ergocalciferol less efficiently; IMPORTANT: Cholecalciferol is highly toxic at overdose in dogs and cats — excess Calcitriol → hypercalcaemia + hyperphosphataemia → metastatic soft tissue calcification (kidneys, aorta, lungs, gastric mucosa − calcium deposits in soft tissues); supplement as directed — do not exceed recommended dose
Indications
- Calcium deficiency (hypocalcaemia) — dietary calcium inadequacy in growing puppies, kittens, and adult dogs and cats on unbalanced home-cooked or all-meat diets (which are inherently calcium-deficient and have an inverse Ca:P ratio)
- Eclampsia (puerperal tetany / puerperal hypocalcaemia) — periparturient hypocalcaemia in lactating bitches (especially small breeds nursing large litters) due to massive calcium loss in milk exceeding dietary intake and skeletal mobilisation capacity; CRITICAL: acute eclampsia requires IV calcium gluconate therapy; Ascal Pet syrup is appropriate for prevention and mild supplementation in at-risk animals, not for acute tetanic crisis management
- Growing puppies and kittens — calcium supplementation to support rapid skeletal growth; NOTE: supplementation in large and giant breed puppies fed balanced commercial diets should only be under veterinary guidance — excess calcium in large breed puppies impairs endochondral ossification and increases risk of developmental orthopaedic disease (DOD: osteochondrosis, hypertrophic osteodystrophy, angular limb deformities)
- Pregnant bitches and queens — meeting increased calcium demand during foetal skeletal mineralisation in the third trimester
- Senior pets — age-related bone density loss and increased fracture risk; calcium supplementation alongside Vitamin D3 supports maintenance of bone mineral density
- Recovery from bone fractures and orthopaedic surgery — adjunctive calcium support during callus formation and bone remodelling
Dosage & Administration
- Shake well before each use
- Administer orally by syringe directly into the mouth or mix into food
- Dose strictly as directed by veterinarian based on body weight, life stage, and clinical indication
- Do not exceed recommended dose — hypervitaminosis D3 and hypercalcaemia are serious risks of oversupplementation
Safety Information
- Avoid calcium oversupplementation in large and giant breed puppies — excess calcium impairs endochondral ossification → developmental orthopaedic disease
- Use with caution in animals with renal impairment (CKD) — impaired phosphorus excretion and altered calcium-phosphorus-PTH axis requires careful management; confirm supplementation need and dose with veterinarian
- Cholecalciferol (Vitamin D3) is toxic in overdose — do not administer more than the veterinarian-directed dose
- Store in a cool, dry place away from direct sunlight; shake well before use; keep tightly capped